High blood pressure is a medical condition where there is abnormal elevation of the blood pressure and this can have serious health consequences.

HTN (hypertension) is the medical term for high blood pressure. Blood pressure is the pressure imparted by the flowing blood on the walls of the blood vessels and for the routine evaluation of your health basically two types of them; systolic & diastolic are measured. Systolic is the maximum pressure created in the blood vessels and corresponds to the contraction of the heart on the other hand diastolic is the minimum pressure created in the blood vessels and corresponds to the relaxation of the heart.

Blood pressure is measured by an instrument called as sphygmomanometer and it is expressed as mmHg (millimeter of mercury).

Grades of HTN

Normal blood pressure (BP) for adults is systolic <120 & diastolic <80 and usually written as 120/80 mmHg by health personnel.

Anything above this range is called HTN and if persistent is considered as chronic HTN. The following grading of HTN is used by doctors to assess the severity of a patient’s blood pressure

* Pre-HTN (120 to 139 or 80 to 89)
* Stage 1 HTN (140 to 159 or 90 to 99)
* Stage 2 HTN (?160 or ?100)
* Isolated systolic HTN (?140 and <90)

How does HTN develop?

To properly understand the mechanisms of development of HTN first we need to familiarize with the mechanisms that maintain the normal blood pressure.

Maintenance of normal blood pressure is a very intricate and at the same sophisticated mechanism that involves different organs, tissues and myriad chemical factors.

The organs involved include;

* Heart
* Kidneys
* Lungs
* Adrenal glands etc.

The tissues involved include

* Blood vessels
* Autonomic nervous system etc.

* The chemical factors include;

* Epinephrine, nor-epinephrine, dopamine
* Renin-angiotensin
* Aldosterone
* Electrolytes like sodium chloride etc.

Arterial blood pressure is determined by two factors including;

* Cardiac output (CO) &
* Peripheral vascular resistance (PVR).

CO is the amount of blood pumped out from the left ventricle to the arterial system per minute and this is determined by;

* Stroke volume &
* Heart rate.

Stroke volume is the amount of blood ejected out from the left ventricle per systole (ventricular contraction) and this multiplied by the heart rate (the total number of heart beats/minute) gives the CO.

PVR is the term used for the resistance exerted by smaller diameter branches of the arteries called as arterioles for the flow of blood through them.

Normally a fine balance is maintained between the CO & PVR so that the blood pressure remains within a healthy range.

The CO & PVR are regulated by interlinked systems like autonomic nervous system & rennin-angiotensin system etc and assist in regulation of the blood pressure. However their over activity can result in HTN.

Autonomic nervous system:

The higher centers for ANS are located in the brain as well as spinal cord. These centers are connected to the target tissues and organs like blood vessels and heart though peripheral & cranial nerves. There are two subdivisions of ANS including sympathetic & parasympathetic systems. The sympathetic division tries to elevate the blood pressure by various mechanisms where as the parasympathetic tries to do the opposite. The sympathetic system works in conjunction with neuro-chemicals like epinephrine, nor-epinephrine dopamine, and acetylcholine whereas parasympathetic system does so with acetylcholine.

Sympathetic nervous system through the above neuro-chemicals increases the heart rate, stroke volume and hence the CO and also constricts the arterioles and increases the PVR and the net effect is an increase in blood pressure. The parasympathetic and sympathetic divisions have opposing actions however the outcome is a normal cardiovascular functioning including heart rate, CO, PVR and the BP.

Renin-angiotensin is another major mechanism involved in the control of BP and it involves kidneys and lungs. Kidney secretes an enzyme called as rennin that cleaves angiotensin I from a protein substrate. Angiotensin I gets converted into angiotensin II in the lungs and this substance is a powerful constrictor of arterioles. Also angiotensin II promotes the release of aldosterone from adrenal gland and this hormone tries to up the sodium concentration in the blood by decreasing its excretion as well as re-absorption in the kidneys.

Adrenal gland is a small organ one on each side that sits on the top of the kidneys. These glands are considered as part of the sympathetic nervous system (the adrenal medulla). The medulla secretes epinephrine and the cortex secretes mineralocorticoids including aldosterone and these hormones as mentioned above will strive to up the BP by various mechanisms.

As you see there are multitudinous structures, chemicals and a very intricate mechanisms involved and if there is disruption in the balance among these different factors then it can result in HTN. And if they are persistent then it may result in chronic HTN.

Consequences (complications) of HTN

Chronic hypertension is a major killer and also condemns the sufferer to a legion of non-death complications. It affects many of the organs & tissues in the body. The chronic extra pressure on the arteries and organs like heart produces several serious pathological changes and predisposes the patient for serious consequences.

Chronic hypertension is one of the risk factors for the development of a process called atherosclerosis in which the inner layers of the arteries are deposited with a type of fat called as cholesterol. This thickening may give rise to blockage of that artery (thrombosis) or the thrombus material may break up and the resulting small fragments (emboli) move distally along the arterial flow and cause blockage called as embolism. Both thrombosis and embolism can produce major organ damages in the form of strokes, heart attack etc.

HTN means heart has to work more because now it has to pump its blood against a high resistance arterial compartment and this extra work results in chronic damage. This can result in angina, heart attack, heart failure etc.

Kidneys are another vital organs that are susceptible to HTN and this may result in ESRD (end stage renal = kidney disease).

Classification of HTN

HTN based on what causes it is broadly classified into either;

* Primary (essential) HTN or
* Secondary HTN.

Primary HTN is the commonest type of chronic HTN and accounts for about 90% of all chronic HTN cases and is supposed to be the outcome of genetic & environmental factors. Its incidence increases with age.

The secondary HTN are the result of certain known pathologies and examples include;

* Kidney related (polycystic kidney disease, kidney tumors etc)
* Adrenal gland (e.g. Cushing’s syndrome)
* Coarctation of aorta
* Obstructive sleep apnea
* Hyperthyroidism
* Pregnancy (/pre-eclampsia/ eclampsia)
* Mediations (e.g. steroids like prednisolone)
* Illicit drugs (e.g. cocaine) etc.

Few special hypertensive situations:

* Malignant HTN
* Hypertensive encephalopathy etc.
In malignant HTN there is severe rise in blood pressure with end organ damage (hypertensive injury to heart, brain, kidney, eyes etc). The patient will present with severe HTN along with findings suggestive of end organ damage like papilloedema (eye changes), blood in the urine, kidney failure etc with kidney involvement, hypertensive encephalopathy (due to brain involvement including clouding of consciousness, seizures, coma etc).

Clinical manifestations

The nonspecific symptoms of HTN include;

* Tiredness
* Decreased exercise tolerance
* Low grade diffuse headache etc.

Specific symptoms due to the particular organ involved include;

* Heart – chest pain, shortness of breath
* Stroke (paralysis of limbs
* Kidney (decreased urine output)
* Eyes- retinal damage decreased vision/blindness etc.

The examination findings include;

* HTN (elevated BP as described above)
* Retinal changes (hypertensive retinopathy)
* Weak peripheral pulses (if atherosclerosis changes have developed)
* Changes in the heart beats (related to ventricular hypertrophy) etc.

Diagnosis

HTN is a clinical diagnosis however certain investigations may be necessary during the evaluation of this condition for example to find out;

* Whether HTN is primary or secondary
* Any end organ damage occurred etc.

Initial investigations generally include;

* Blood electrolytes
* Urine analysis
* ECG
* Echocardiogram

Blood electrolytes like sodium, potassium, chloride, BUN, creatinine, calcium etc are measured and generally measure the functional integrity of kidneys that might have been affected by HTN. There may be mineralocorticoid secreting tumors that caused HTN then serum sodium is elevated and potassium is decreased.

During urine analysis you will look for;

* Abnormal albumin excretion
* Abnormal creatinine clearance
* Renal casts etc.

These tests come abnormal in varieties of kidney pathologies however in an appropriate setting they might indicate hypertensive kidney damage.

ECG might show changes suggestive of heart damage secondary to ischemia (decreased blood supply) that may be due to long standing HTN. A left ventricular strain pattern may be seen in the form of depression of ST segment and inversion of T wave in the left precordial leads. Tall QRS complexes are frequently seen too and suggestive of left ventricular hypertrophy. Changes suggestive of prior heart attack etc may serve as an indirect evidence for hypertensive ischemia of the heart.

Echocardiogram will show structural abnormalities in including left ventricular hypertrophy, regional wall decreased movements suggestive of previous heart attack etc.

If we are suspecting secondary hypertension then a meticulous search for the cause of HTN is necessary and some of the investigations obtained include;

Pheochromocytoma tests (blood/urine catecholamine, imaging studies of adrenal glands etc)
Renal artery narrowing(angiogram of renal artery, blood & urine tests related with kidney damage)
Coarctation of aorta (angiogram of aorta etc)

Management of HTN

The HTN management is generally dealt in the following lines including;

1) Acute HTN management
2) Chronic HTN management (non-mediation approaches)
3) Chronic HTN (medication approaches)
4) Treating the cause for secondary HTN

1) Acute severe HTN, medications used include:

Labetalol
Nicardipin
Nitroprusside
Phentolamine
Nitroprusside
Nitroglycerin etc.

When blood pressure is severely elevated then it is recommended not to bring it down too quickly rather to be done slowly and immediately after an ischemic stroke the high blood pressure is supposed to be left a it is unless is a crisis situation.

2) Chronic HTN, non-medication management (lifestyle modification etc);

Dietary salt restriction about <6 g/day
Weight reduction
Low fat, high fiber, vegetable, fruit diet
Alcohol abstinence or in small quantity only
Cessation of smoking
Regular adequate exercise etc.

3) Chronic HTN management (medication approaches) include;

* Centrally acting / a2 agonists;

Methyl Dopa
Clonidine

* Adrenergic blockers:

Alpha blockers (Phenoxybnzamine, Phentolamine, Prazosin, Terazosin etc)
Beta blockers (Metoprolol, Atenolol, Propranolol etc)
Both alpha and beta blockers (Labetolol, Carvedilol etc)

* ACE inhibitors;

Enalapril
Lisinopril
Ramipril
Trandolapril etc.

* Angiotensin 2 receptor blockers (ARBs);

Candesartan
Losartan
Valsartan etc.

* Vasodilators;

Arteriolar vasodilators (calcium channel blockers like Amlodipine etc)
Non calcium channel blocker arteriolar dilators like hydralazine
Aterio venular vasodilators like sodium Nitroprusside

* Diuretics;

Furosemide
Hydrochlorthiazide (HCTZ)
Amiloride + HCTZ etc.

4) Treating the causes for secondary HTN depending upon what caused it may include  discontinuation or reduction in the dosage of glucocorticoids (steroids), treating pheochromocytma, coarctation of aorta, kidney pathologies etc.

Cardiomyopathies are a group of diseases involving primarily the heart muscle and by definition they must not be the result of one of the following causes;

• Congenital (present at birth)
• High blood pressure
• Acquired valvular
• Ischemic (coronary artery related- heart attack)
• Pericardial abnormalities

Classification

Cardiomyopathies are classified based on morphological features under these three categories including;

• Dilated (D)
• Restrictive (R)
• Hypertrophic (H) types.

Then depending upon what causes them they are further classified into two categories as below;

• Primary &
• Secondary types.

In the primary types you see these sub categories;

• Idiopathic D, R or H types (cause unknown)
• Familial (hereditary) D, R, or H types
• Endomyocardial fibrosis (R type)
• Eosinophilic endomyocardial disease (R type)

The secondary type is a result of a known cause like a systemic disease for example and they can be further categorized as below;

• Dilated
  • Infective (bacterial, viral, protozoal, fungal, spirochetal, ricketsial etc)
  • Neuromuscular (myotonic dystrophy, muscular dystrophy etc)
  • Deficiency related (nutritional & electrolyte deficiency)
  • Metabolic cardiomyopathies
  • Hereditary storage disorders (glycogen storage disorders etc)
  • Connective tissues disorders (lupus, dermatomyositis etc)
  • Infiltrative conditions (sarcoidosis, amyloidosis etc)
  • Toxin exposure (radiation, alcohol, drugs etc)
  • Peripartum cardiac disease

• Restrictive
  • Hereditary storage disorders (glycogen storage disorders etc)
  • Infiltrative conditions (sarcoidosis, amyloidosis etc)

• Hypertrophic (Friedreich’s ataxia)

Please note that certain causes can give rise to more than one type of cardiomyopathy, for example a familial storage disorder like glycogen storage disease may induce either a dilated or restrictive cardiomyopathy or both in combination.

Dilated cardiomyopathies (DCM):

About 20 to 30% cases of DCM are hereditary in nature and rest is either idiopathic or related with some causes mentioned as above.

Clinical course: Although initially majority of the patients are asymptomatic eventually they become symptomatic & progressive. Some patients may stabilize spontaneously but for the rest it is a relentlessly downhill course and they succumb to the disease in the next few years or so.

The complications & death are generally due to the development of

• Heart failure (HF)
• Cardiac arrhythmias etc.

Clinical features:

• Progressively downhill course
• Chest pain (vague & not typical for angina)
• Syncope (fainting)
• Manifestations of heart failure
  • shortness of breath,
  • swelling of limbs,
  • ascitis (fluid accumulation in the abdominal cavity)
  • syncope (fainting),
  • generalized weakness, fatigue
  • malaise feeling
  • loss of appetite
  • decreased urine out put
  • embolic phenomena like strokes etc
• Manifestations of cardiac arrhythmias
  • syncope (fainting)
  • embolic phenomena like strokes due to clot generation in the heart chambers
• Sudden cardiac death (SCD) syndrome

Diagnosis:

• ECG
• Echocardiogram
• Cardiac catheterization and coronary angiography etc.

ECG studies the electrical activities generated from the heart. Echocardiogram is an ultrasound technique of visualizing the heart structures and its functions. Cardiac catheterization & coronary angiography are invasive procedures involving passing a catheter to the heat chambers and the major vessels like aorta & pulmonary arteries and studying their anatomy and functions.

The above tests will help with identifying cardiomyopathies and their classification.

Management:

• No specific or curative treatment available as of now
• Supportive and symptomatic care
• Avoiding strenuous exercise & physical exertion
• Blood thinness (warfarin) to reduce complications of clot (embolism)
• Treat heart failure & cardiac arrhythmias appropriately
• Avoid toxins & drugs like alcohol, non-steroidal pain killers as much as possible
• Healthy lifestyle including tolerable exercise, good nutrition
• Heart transplantation for advanced stage of the disease

Restrictive cardimyopathies:

As the name implies there is a phenomena of restriction and this occurs to the blood filling of the heart chambers especially the ventricles. The ventricular walls are abnormally rigid due to pathologies including fibrosis, infiltration or hypertrophy due to myriad causes. The result is a deficient filling of blood in the heart which means heart will pump out less blood to meet the demands of the body so the tissues and organs will be undernourished. Also more blood pools in the body as its return to the heart is hindered.

The clinical picture, course, and management approach are all in general similar to DCM as there is a global dysfunction of the heart and eventually they develop complications like HF, cardiac arrhythmias & clot formation (systemic embolism) etc.

The restrictive cardiomyopathy associated with hemochromatosis (iron overload) carries a better prognosis as once it is identified the iron overload can be kept under control. For other varieties the course is downhill as DCM.

Hypertrophic cardiomyopathies:

Its incidence in the general population is about 1 in 500 and the two most characteristic features of this condition include;

• Preferential hypertrophy of inter-ventricular septum
• The sub aortic narrowing (stenosis) causing dynamic pressure gradient

About 50% of patients have a genetic cause in the form of family history.

Clinical picture & course:

• Some are asymptomatic
• Some present with only mild symptoms
• Sudden cardiac death (SCD) syndrome is common in children and adolescents
• Angina type chest pain occurs
• A typical harsh systolic murmur is frequently heard corresponding to aortic origin
• Heart failure & cardiac arrhythmias can occur

Investigations:

• ECG (shows left ventricular hypertrophy)
• Echocardiogram (confirms left ventricular and septal hypertrophy)
• Chest x ray may show a large heart
• ECG and/or Echo will also show complications like
  • Heart failure
  • Cardiac arrhythmias etc.

Management:

• Strenuous activities & competitive sports are to be avoided
• Avoid dehydration, use of diuretics etc
• Medications generally recommended include
  • beta blockers like metoprolol
  • calcium channel blockers like verapamil
  • anti-arrhythmic agents like amiodarone
• Surgical interventions for hypertrophic septum
• Implantable cardiac defibrillators for patients at high risk for SCD.

Cardiac arrhythmias are the result of abnormal electrical activity in the heart and represent myriad number of such conditions lumped under this broad heading. Their clinical significance ranges from being not concerning at all, to rapidly fatal if not identified and treated quickly.

The normal heart rate is around 60 to 100 /minute in adults and it is considered rhythmic, what it means is the time interval between the subsequent heart beats should be the same. By and large that is how it is, although a minor variation called as sinus arrhythmia is seen and this is related with breathing; during the inhalation of air the heart rate increases slightly and the opposite with exhalation.

Other than this phenomenon if the rhythm of the heart beats is lost or the rate of heart beats is below or above the normal range it is called as cardiac arrhythmia.

Mechanism of arrhythmia development

The physical activity of the heart related with its receiving in & pumping out of blood is mediated by the underlying electrical activities.

These electrical activities normally originate in a structure called as SA node (sino-atrial) and it is the normal pacemaker of the heart. The impulses from here reach the atria as well as another nodular structure called as AV node (atrio-ventricular). From the AV node the impulses travel initially through the ‘bundle of his’ then through its right & left branches and subsequently through structures named as purkinje fibers and supply the whole ventricles.

The basic pathology for the development of cardiac arrhythmias lies in the abnormalities of electrical impulse generation, its propagation or both and it can occur anywhere along the structures mentioned above.

Various pathologies contribute for the development of arrhythmias including;

• Fibrosis
• Electrolyte abnormalities
• Infections
• Inflammatory conditions etc.

The important basic cellular mechanisms promoting the arrhythmias include;

• Abnormal conduction of impulses (reentry) – the commonest cause
• Development of abnormal automaticity
• Abnormal after depolarization & triggered firing etc.

Types & classification

Cardiac arrhythmias are broadly lumped under two categories including;

• Tachy-arrhythmias (fast heart rate) &
• Brady-arrhythmias (slow heart rate)

Tachy-arrhythmias:

• Premature complexes (atrial or ventricular)
• Junctional premature complexes
• Sinus tachycardia (due to fever, stress, thyrotoxicosis, anemia, hypotension etc)
• Tachycardia (atrial or ventricular)
• Multi-focal atrial tachycardia
• AV nodal tachycardia
• AV junctional tachycardia
• Tachycardia related to abnormal accessory pathways (WPW syndrome)
• Flutter (atrial or ventricular)
• Fibrillation (atrial or ventricular)

Brady arrhythmias:

• Sinus bradycardia
• Sinus pauses
• Sinus arrest
• Sinus exit blocks
• Atrio-ventricular conduction blocks (1st 2nd or 3r degree)

Diagnosis

Investigations helpful for the identification and management of arrhythmias include;

• ECG
• Holter monitor, Event recorder, Loop recorder etc
• Echocardiogram
• Blood tests
• Electrophysiological study etc.

The ECG studies the electrical activities originating from the heart and is of immense value as to the identification & classification of arrhythmias. It is easily available and relatively inexpensive too.

However if the arrhythmias are infrequent then you need longer recording and this is usually accomplished with Holter monitor, event recorder or loop recorders.

For holter monitoring the chest ECG electrodes are connected to a small portable box and recording of the ECG is continuous. Even monitor is some what similar to holter monitor although the recording is not continuous and patient will push a button during events and recording takes place during that time only. Event monitor is needed when the events are rarer to be captured by holter and ILR is generally needed when events are still rarer to be recorded even by event monitor. ILR is inserted under the skin on the left side of chest near to the heart and recording is done.

Echocardiogram is an ultrasound technique for visualizing the heart as to its chambers, valves, blood flow etc. It may give clues to various cardiac abnormalities which are associated with cardiac arrhythmias including; heart attack, left atrial dilatation (especially due to rheumatic heart disease) etc.

The electrophysiological test is a highly advanced procedure for the evaluation of cardiac arrhythmias. During the procedure a catheter is passed through the blood vessels in to the heart chambers and electrical activities are analyzed by methods including electrical stimulation and administering drugs that can cause arrhythmias. If the source of the arrhythmia is detected then a procedure called as radiofrequency ablation may be performed as a treatment too.

During blood tests you look for electrolyte abnormalities, thyroid function, infection etc that may have contributed to the development of arrhythmias.

Management

The cardiac arrhythmias are heterogeneous with regard to their origin, nature and clinical relevance, and the management too varies depending upon the arrhythmia type.

The following are the different management options available and the selection of the treatment modes is done on a case-by-case basis.

• Vagal nerve stimulation technique
  • Valsalva maneuver
  • Carotid sinus massage
• Medications (anti-arrhythmic drugs)
• Electrical cardio-version (for a-fib, a-flutter, v-tach etc)
• Defibrillation (for cardiac arrest with v-fib, other v-fibs, pulse less v-tach)
• Surgical treatments
• Electrophysiological interventions (ablation therapy)
• Treat the underlying causes of arrhythmias
• Management of complications resulting from arrhythmias

Anti-arrhythmic medications:

Class 1:  (sodium channel blockers)

• 1a – procainamide
• 1b –Lignocaine
• 1c – flecainide

Class II (beta blockers): propranolol, metoprolol etc

Class III (potassium channel blockers): amiodarone

Class IV (calcium channel blockers): diltiazem

Class V (work by other mechanisms): e.g. adenosine

Some of these above drugs may display more than one mechanism.

• Atropine for brady-arrhythmias

Surgical treatments:

• Implantable cardiac pacemakers, defibrillators etc.

Treat the underlying causes;

• Hyperthyroidism
• Electrolyte abnormalities
• Infections etc.

Management of complications associated with arrhythmias;

• Clot management (use blood thinners);
  • Intravenous heparin
  • Warfarin
• Heart failure management (treated along the standard lines)
• Cardiac arrest (treated along the standard lines)

Infective endocarditis (IE) is a serious form of heart disease where there is infection of the endocardium (the inner aspect of the heart chambers) by microorganisms.

This condition needs to be identified quickly and treated aggressively to save the patient from death or serious heart complications.

Structures Involved

These structures or areas of the endocardium may get involved either alone or in combination;

• Heart valves (native)
• Heart valves (prosthetic)
• Mural endocardium
• Intra-cardiac devices

The heart valves are structures that serve as one way gates between the two chambers of the heart on right or left side, also between the ventricles and pulmonary artery or aorta. Native heart valves are the valves a person was born with and prosthetic ones are the artificial valves. Mural endocardium is the thin structure that lines the inner surface of the heart. Examples of intra-cardiac devices include implanted defibrillator, transvenous pacemaker lead etc.

What organisms cause IE?

The organisms mostly responsible for IE are

• Bacteria &
• Fungi

Most of the IE is caused by bacteria; and many different types of bacteria are involved with the IE and few of the common ones are;

• Streptococci
• Staphylococci
• HACEK organisms
• Pseudomonas etc.

What situations predispose these infections?

• Prior damage to the endocardium, such as
  • Rheumatic heart disease
  • Congenital heart diseases etc
• Recent surgical interventions related with the heart
• IVDA (Intravenous drug abuse) etc.

The normal intact endocardium is highly resistant to infection however the above mentioned situations promote the invasion of the pathogens to the endocardial structures including the valves. Initially there a development of what we call as NBTE (nonbacterial thrombotic endocarditis) which is a sterile clot or thrombus like structure that attaches to these damaged areas. When there is an invasion of microorganisms into the blood stream and as they move across these NBTE structures these organisms may attach themselves to NBTE and such NBTE is called as vegetations as they contain the pathogens. These vegetations are the hallmark features of IE.

The microorganisms in the vegetations divide and grow in number and initiate an inflammatory response and this will produce additional damage to the already   compromised structures. Patients usually develop new murmurs related with this new damage. This will put extra burden on the heart muscle and in severe cases will result in heart failure (HF).

Also the vegetations can break from the endocardium and enter the arterial circulation and reach other organs like brain. They may block the arterial branches and can result in conditions like stroke. Sometimes the blockage of arteries by infected vegetations may result in damage to the arterial walls and may result in what is called as mycotic aneurysms. They may rupture causing bleeding in to the organ especially the brain.

Types

Infective especially the bacterial endocarditis is traditionally classified as acute & sub acute bacterial endocarditis (SABE) based on the evolution of clinical manifestations. The more virulent organisms cause more severe damage to the valves and results in earlier onset of clinical manifestation and rapid progression of the disease process. SABE presents & progresses somewhat slowly.

Clinical manifestation

Generally patients present with these manifestations including (not all patients);

• Fever
• Sweating & chills
• Loss appetite and loss of weight
• Malaise (ill feeling)
• Joint & muscle pain
• Heart murmurs
• Osler’s nodes, subungual hemorrhages, spleen enlargement etc
• Manifestation related to the complications (e.g. stroke, seizures)

Diagnosis

Duke criteria, a set of clinical criterias used in diagnosing IE, are employed to arrive at the diagnosis with reasonable accuracy and the clinical, blood tests and echocardiograpic findings are used here.

There are two major & five minor criteria.

The major criteria include;

• Positive blood culture
• Proof that endocardium is indeed involved
  • Abnormal echocardiogram
  • Evidence for the involvement of a new murmur

Minor criteria include;

• Predisposing conditions (preexisting heart problems, intravenous illicit drug abuse)
• Presence of fever (temp equal or more than 38.0 degrees)
• Vascular manifestations
• Immunological manifestations
• A positive blood culture or serological proof of active infection

A clinical diagnosis of definite IE is made if one of the following is fulfilled;

• Two major criteria
• One major + three minor criteria
• Five minor criteria

Possible IE if one of the following is fulfilled;

• One major + one minor criterion
• Three minor criteria

The blood culture, if comes positive will assist with the diagnosis as well as with choosing the appropriate antibiotics through culture sensitivity. The echocardiogram uses ultrasound technique to visualize the heart chambers, valves, blood flow etc of the heart. The endocarditic vegetations may be seen. Generally TTE (trans-thoracic echo) is performed however TEE (trans-esophageal) is more sensitive for smaller vegetations.

Management

The management of IE includes the following;

• Empirical antibiotic treatment
• Specific antibiotic treatment
• Symptomatic treatment
• Treatment of complications
• Surgical treatment etc.

Initially if the exact causative organism is not known then a combinational empirical antibiotic course is initiated. If the culture grows & identifies the pathogen then only specific antibiotics can be tried based on antibiotic sensitivity information. The initial antibiotics generally used include;

• Penicillin
• 3rd or 4th generation intravenous cephalosporins
• Vancomycin
• Gentamicin etc.

Fungal endocarditis is much rare as compared to the bacterial one and amphotericin antibiotic is the mainstay of treatment.

Surgical treatment is employed if medical management fails and includes procedures like removal of the infected valve etc.

Synopsis

Infective endocarditis (IE) is a life threatening illness involving the heart so the diagnosis & treatment both need to be achieved at the earliest.

Rheumatic heart disease (RHD) is one of the serious heart sequelae of usually a childhood disease by name rheumatic fever.

Rheumatic fever (RF) in turn is a complication to infection with the bacteria by name group-A beta hemolytic streptococci; and usually develops one to few weeks after streptococcal throat infection (rarely scarlet fever, a skin disease). It is considered to be an autoimmune disease meaning the body’s immune system; instead of helping the body paradoxically attacks it. During the streptococcal infection certain antibodies are formed and they cross react with various tissues in the body including heart, brain, joints, skin etc and can damage these structures.

Frequency & distribution

Rheumatic fever mostly affects children especially around age 5 and 15. It predominantly occurs in developing countries particularly when there is a prolonged overcrowding of people e.g. low socioeconomic families.

Classification of RHD

Although this classification is not universally used, for the convenience of discussion RHD may be generally divided into two types as below;

• * Acute &
• * Chronic types.

Acute RHD presents as a manifestation of rheumatic fever, it is called as rheumatic carditis, and it is one of the major Jones criteria for the diagnosis of rheumatic fever.

The chronic type is not a new disease as such and it is the long term complication related with any residual cardiac damage especially the valvular damage and generally it begins manifesting few to several years after the acute attack. Recurrent streptococcal infection may occur in some patients especially those who do not take long term penicillin antibiotic and results in accruing of additional damage to the valves.

More about RHD

Acute RHD:

It is a pan-carditis meaning it usually involves all three layers of heart. The inflammation of the three layers of the heart, the pericardium, myocardium & endocardium are respectively called as pericarditis, myocarditis & endocarditis.

The acute rheumatic pericarditis and myocarditis are most often self limiting illnesses and resolve without any sequelae. However patients are not that lucky with the endocarditis as many of these patients develop valvular abnormalities; and even after the acute attack is over the residual or progressive valvular dysfunction can compromise the functioning of the heart and may even result in death if not intervened appropriately.

The acute attack passes away with general & supportive care although some patients may develop heart failure, serious cardiac arrhythmias and even death.

Chronic RHD:

As pointed out above chronic RHD is a result of prior episode of the rheumatic carditis especially the endocarditis and its valvular complications. There are total four heart valves; they are named as below and in the bracket their relative involvement in RHD is shown;

• * Mitral (commonest)
• * Aortic (next common)
• * Tricuspid
• * Pulmonary (least common)

The initial damage to the valves may occur at their cusps, or the chordae tendinae structures or both. This initial endocarditis causes an inflammatory reaction resulting in anatomical changes in these valves and they do not function properly as a result of this. The valves either become stenotic (narrow) or leaky and this alters the normal blood flow pattern from one chamber of the heart to another or from the heart to aorta or pulmonary artery. This will overburden the heart muscle and results in a chronic malfunctioning. Also recurrent streptococcal infections might add on more valve damage, and if that happens, it will only hasten the deterioration of the functioning of the heart.

As the heart function and the blood flow patterns change certain serious consequences might develop including; left atrial dilatation, clot or thrombus development in that chamber, cardiac arrhythmias, abnormal thickening and or dilatation of different heart chambers and the complications like heart failure. The clot formed can break up and the fragments can get pumped out of the heart and block the arterial circulations resulting in stroke etc. The cardiac arrhythmias can also contribute for the formation of the clot and heart failure. Infective endocarditis is another serious and life threatening complication of chronic RHD.

Diagnosis

The diagnosis of RHD is both clinical and investigational and it can be discussed at three levels including;

• Acute RF/RHD
• Chronic RHD
• Complications related with chronic RHD

Acute RF/RHD stage:

Throat swab
Antibody titers (e.g. ASO titers)
ECG
Echocardiogram
Blood tests (discussed under Jones criteria)

When the patient already has presented with acute RHD/rheumatic fever stage the streptococcal infection has been resolved most often. So throat swab to look for streptococcal bacteria is not always going to help. However the bacteria may continue to harbor the throat even after the throat symptoms have subsided so it is worth trying.

Certain antibody tests like ASO titer may be of some assistance too. These antibodies generally appear in the blood within several day of a streptococcal infection and the titer rises gradually for about a month or so. Then the titer remains stable for few months and finally returns to normal gradually within a year or so. If the titer is performed early in the disease, and repeated a couple of weeks later, and if a rise in the titer can be demonstrated it is highly suggestive of recent streptococcal infection.

ECG studies the electrical activities of the heart. Although no diagnostic ECG changes are seen however the presences certain ECG changes as below indicate the involvement of the heart;

• Tachycardia (fast heart rate)
• Bradycardia (slow heart rate)
• Prolonged PR interval
• ST segment elevation if pericarditis is present

Echocardiogram is an ultrasound investigation and used to check the real time images of the heart muscle, heart chambers, valve structures and motion blood flow etc. It is an extremely invaluable investigation for the evaluation of RHD/RF.

For the proper diagnosis of acute RF, revised Jones criteria needed to be employed and there are major & minor criteria as below.

Major criteria;

• * Arthritis
• * Carditis
• * Sydenham’s chorea
• * Subcutaneous nodules
• * Erythema marginatum

Minor criteria;

• * Fever
• * Raised ESR
• * Raised C reactive protein
• * Arthralgia (minor joint pain without swelling)
• * Prolonged P-R interval (on ECG)

The arthritis characteristically involves the large joints of the limbs and usually migrates from one joint to the other. Rheumatic carditis discussed along with acute rheumatic heart disease. Chorea is the term used for certain characteristic rapid, purposeless involuntary movements of the limbs and face and affects girls more than the boys. The rheumatic nodules develop under the skin due to collections of connective tissue like collagen and are typically painless and occur on the back of the elbow, wrists and front aspect the knee joints. The skin rash involves the arms or the trunk which spreads outwards with a pink serpiginous margin and a fading center.

For the diagnosis of acute rheumatic fever you need;

• * Two major criteria OR
• * One major criterion plus two minor criteria AND
• * Evidence for a recent streptococcal infection in the form of one or all of following;

Throat swab positive for streptococci
Raising ASO tires
History of scarlet fever

The presence of rheumatic chorea or indolent carditis can be themselves considered as suggestive of rheumatic fever and do not require other points mentioned with Jones criteria.

Chronic rheumatic heart disease stage:

• * Echocardiogram
• * ECG
• * Cardiac catheterization etc

The role of ECG & echocardiogram is as discussed above. During cardiac catheterization a catheter is passed in to the heart chambers and the anatomy and functioning of the heart valves and other structures studied.

Stage of chronic RHD complications: It is not a distinct stage by itself rather overlaps with the stage of chromic RHD and the complications include;

• * Left atrial dilatation
• * Clot in the heart
• * Cardiac arrhythmias
• * Endocarditis etc.

These conditions are diagnosed by using ECG, echocardiogram, blood cultures etc as necessary.

Management

Management of RHD can be dealt at acute RF & chronic RHD levels.

Acute RF/RHD management;

• * Bed rest
• * Aspirin for pain, fever & inflammation of joints
• * Penicillin antibiotic
• * If chorea is present treat with appropriate medications
• * If heart failure or arrhythmia develops treated accordingly

Penicillin is the antibiotic of choice for streptococcal throat infections. At the time acute RF diagnosis majority of the times the sore throat is better however a course of penicillin is still generally recommended as the bacteria may be still present in the throat and it can spread to close contacts.

Penicillin prophylaxis is recommended for patients who had rheumatic fever; and how long or how often etc depend upon how much heart damage is present. Rheumatic fever has a tendency to recur and such recurrences increase the chances of additional heart valve damage so it is of paramount significance to take penicillin, or a suitable alternative if penicillin allergy is present, for the recommended duration.

Management of chronic RHD & its complications includes (on a case-by-case basis);

• * Valvular surgery (e.g. replacement with a prosthetic valve)
• * Chronic blood thinner treatment
• * Treatment of heart failure
• * Treatment of cardiac arrhythmias
• * Prevention & treatment of infective endocarditis etc.

Heart failure (HF), as the name implies is a general state of failure of heart’s functioning and the resultant inability to keep up with the body needs of blood supply and nutrition.

HF is not a disease by itself rather it is one of the serious late stage manifestations of various disorders of heart that are expressed in the form of an impaired pumping ability of the heart and its untoward consequences. Heart being one of the prime vital organs in the body, its malfunctioning will undoubtedly have serious health ramifications and that is very much true with heart failure too.

Types/ classifications

Heart failure is classified in varieties of ways depending upon;

• The evolution of symptoms;
  • Acute or
  • Chronic heart failure
• The side of the heart involved;
  • Left sided or
  • Right sided or
  • Both sided failure
• The cardiac out put status;
  • Low out put or
  • High out put failure
• The phase of the cardiac cycle mainly affected;
  • Systolic or
  • Diastolic failure

The NYHA (New York Heart Association) Functional Classification looks at the functional abilities of these patients and include;

• Class IV: most severe form, symptoms occur even at rest
• Class III: Only rest makes patients comfortable, not any activity
• Class II:  Minor limitations of activities
• Class I:   Quite stable patients, no symptoms from routine activities

Risk factors for Heart Failure

Any pathological condition that can negatively influence the pumping action of the heart muscle may precipitate low out put HF and several such conditions include;

• Ischemic heart disease (heart attack)
• Cardiomyopathies
• Cardiac arrhythmias etc.

Generally the following factors contribute to the development of above mentioned conditions;

• Valve abnormalities (e.g. rheumatic heart disease)
• Smoking
• High blood pressure
• Diabetes
• High cholesterol etc.

The other type of HF, the high out put one initially will present with an increased ejection fraction of blood however this is an abnormal state and in the process the heart muscle gets overburdened and gradually it fails and eventually manifests as low out put HF. The conditions giving rise to high out put HF include;

• Severe anemic states
• Aortic regurgitation
• Arterio-venous shunting
• Fever
• Thiamine (Vitamin B1) deficiency state – beriberi etc.

The above discussion is generally for either left heart failure or a combination of both left & right heart failures. There are conditions that will present with isolated right heart failure and the term Cor pulmonale is used if this right HF is secondary to lung pathologies like chronic bronchitis, emphysema etc.

Clinical manifestations

The following are common clinical feature (not every patient will present with all these features);

• Difficulty with breathing
• Edema (swelling of legs)
• Ascitis (distension of abdomen due to fluid accumulation)
• Generalized weakness & fatigue
• Chest pain (angina)
• Jaundice (rare)
• Wide pulse pressure
• Aortic regurgitation murmurs
• Abnormal lung auscultation findings (e.g. rales)

Diagnosis

The investigations generally required for the confirmation of HF and its further management include;

• Echocardiogram
• ECG
• Chest x-ray
• Cardiac catheterization
• Coronary angiogram
• Blood tests (cardiac markers, natriuretic peptides etc)

Echocardiogram is an ultrasound technique for imaging the heart. The role of this test in the diagnosis of HF is invaluable. It provides a clue regarding the global functioning of the heart, including its wall motion, chamber size, valve function, blood flow etc. It gives us a measure of the EF (ejection fraction) which is the most useful index of left ventricular function. An EF equal or above 50% is considered adequate and it is considered significantly depressed when values are < 30 to 40%.

ECG records the electrical activities of the heart and may provide clues regarding what might have precipitated HF for example heart attack, arrhythmias etc.

Blood tests:

The cardiac markers usually checked include;

• Total CPK
• CPK MB fraction
• Troponin

These tests will reveal if any heart attack had occurred recently. The natriuretic peptides are usually elevated in HF.

Cardiac catheterization & coronary angiograms are generally performed together. These tests will detect conditions like cardiomyopathies, ischemic heart disease etc that might have precipitated HF.

A catheter is passed through an artery like femoral artery and advanced to the aorta and a radioactive dye in injected such that it enters the coronary arteries and the radiological pictures are taken to look for a blockage. If required the catheter from the aorta is advanced to the left heart for additional evaluation.

Management

1) Acute setting;

• Bed rest (for short duration)
• Injection Lasix (Furesemide) to get rid of excessive water from the body
• Oxygen supplementation (nasal or through breathing machine as necessary)
• Fluid restriction
• Salt restriction
• Measures to avoid blood clots in the legs due to bed rest
  • Low molecular heparin injections
  • Intravenous heparin
• Identifying and treating what precipitated or caused HF;
  • Heart attack
  • Cardiac arrhythmias
  • Infections
  • Medications
  • Noncompliance with fluid and salt restrictions
  • Poor control of blood pressure etc.
• Nitrate preparations for reducing the work load of the failing heart
• Nitrate preparations and/or morphine for chest pain/discomfort
• Medications to enhance the pumping action of the heart muscle:
  • Inj Dobutamine
  • Inj Dopamine
  • Inj Milrinone
• Medication to constrict arteries (if blood pressure is too low)
  • Inj Dopamine
  • Inj Epinephrine
• Ultra filtration
• Dialysis etc.

2) Long term or maintenance therapy includes;

• Salt restriction
• Fluid restriction
• Tolerable amount of exercise
• Lifestyle modification like cessation of smoking etc
• Medications like;
  • Anti-platelet agents (aspirin, clopidogrel)
  • Blood thinners like warfarin if there is clot risk developing in the heart
  • Angiotensin converting enzyme inhibitors like lisinopil
  • Angiotensin receptor blockers like candesertan
  • Aldosterone antagonists like eplerenon
  • Digoxin
  • Antiarrhythmic agents like amiodarone (if arrhythmias are present)
• Cardiac resynchronization therapy (if ventricular asynchrony is present)
• Implantable cardiac defibrillator (if refractory arrhythmias are present)
• Cardiac transplantation (generally one of the last measures)

Angina is defined as a chest pain that is mostly transient and usually episodic and results secondary to a reduction in the arterial blood supply to the heart.

Along with heart attack it is grouped under CAD (coronary artery diseases) or IHD (ischemic heart diseases) as both these conditions are the result of blockage of coronary arteries that supply heart. Angina is classified as stable or unstable; stable angina is a manifestation of chronic CAD where as unstable angina is appropriately dealt with acute CAD (called as acute coronary syndrome) as its clinical evolution, implications & management aspects are different than that of stable angina.

Risk factors

The risk factors for the development of angina include;

• High blood pressure (HTN)
• Diabetes mellitus
• Smoking
• High cholesterol (the bad cholesterol like LDL)
• Decreased good cholesterol (HDL)
• Elevated triglycerides
• History of heart disease in the family
• Increasing age
• Obesity
• Oral contraceptive pills (OCP)

We do not have a control on certain risk factors like aging, family history etc but most other risk factors are under our control, at least to some extent, like leading a healthy life style, adieu to smoking, sincere attempt to control medical conditions like HTN, DM etc.

How does angina attack develop or happen?

The angina attack is the result of a partial or reversible decreased blood supply to an area of heart muscle. The body cells are dependent on the arterial blood flow for their nutritional supply including the fuels like glucose for energy production, oxygen for various metabolic activities and myriad other nutrients to maintain the well being and functioning of the cells.

When a sudden reduction in the arterial blood flow takes place the heart cells cannot sustain their function properly and clinically this may manifest as chest pain.

The blockage in an artery especially with the coronary arteries supplying the heart is mostly due to a condition called as atherosclerosis.  This is a gradual process developing over several years during which generally a progressive accumulation of cholesterol takes place on the inner margins of the arteries. Certain blood cells called as platelets and macrophages (cells like monocytes normally help in fighting infections) also take part in this process. This abnormal build up continues provided the patients do not do anything to halt it and a time may come when it starts compromising the blood flow in that artery. If it is partially occluding the artery then reversible or minor symptoms like angina occurs on the other hand if the blockage is complete it may result in the severe form, the heart attack.

Clinical manifestations

The location of angina is generally over the left chest and has a tendency to radiate to the arms and shoulders especially on the let side. It may also radiate to epigastric region, jaw, teeth, back etc. Patients may not always describe this as some frank pain rather they use various terms like pressure, heavy, squeezing, smothering like feelings and the duration is usually between 2 and 5 minutes.

Generally these attacks are precipitated by physical exertion or emotional and relieved with rest and relaxing but can occur at rest & while relaxed too.

On examination patients do not usually reveal any abnormal findings per se related with the angina.

Diagnosis

Angina is a clinical diagnosis although not always this can be attained by clinical criteria alone. If patients present with characteristic manifestations it becomes straightforward otherwise it is not easy to clinch the diagnosis clinically. Also there are other clinical conditions that can manifest with chest pain mimicking an angina.

The investigations ordered during the evaluation of stable angina include;

• ECG
• Blood tests

Additional tests;

• Echocardiogram
• Cardiac stress test
• Holter monitor
• Coronary angiogram
• Cardiac catheterization etc.

ECG records the electrical activities of the heart, and angina may produce certain important ECG changes with T waves & ST segments, although not necessarily specific for angina; however in a proper clinical setting they may have diagnostic values.

Blood tests are done to look for medical conditions that impart the risk for ischemic heart diseases e.g. diabetes, high cholesterol etc.

Echocardiogram is an ultrasound technique for imaging the heart. It may not aid in the diagnosis of an angina attack however this test may provide a clue regarding the     global functioning of the heart, including its wall motion, chamber size, valve function, blood flow etc. It can also tell us if the patient had a prior heart attack (decreased regional wall motion). It may be performed in conjunction with a cardiac stress test as well.

Cardiac stress test: This test evaluates the adequacy of coronary artery blood supply to the heart while heart is put under stress. Patient’s baseline cardiac parameters like blood pressure, heart rate, ECG are documented. The cardiac stress is induced by asking the patient to do exercise (usually treadmill) or by injecting certain drugs. During these stressors the ability of coronary arteries to meet the nutritional demands of the heart muscle is studied. Injecting radioisotopes seems to increase the sensitivity & specificity of the test.

Cardiac catheterization & coronary angiograms are not routinely ordered for typical stable angina.  It is required only if;

• Diagnosis is uncertain
• Severe angina patients who may require special interventions like;
  • PCI (primary coronary intervention)
  • CABG (coronary artery bypass grafting) etc.

A catheter is passed through an artery like femoral artery and advanced to the aorta and a radioactive dye in injected such that it enters the coronary arteries and the radiological pictures are taken to look for any blockage. If required the catheter from the aorta is advanced to the left heart for additional evaluation.

Management

The acute or immediate management approach of stable angina includes the following measures;

• Reassurance to the patient
• Treatment of angina pain with nitrate preparations (sublingual, oral etc)

Long term therapy or preventive measures include (not every patient requires each of these interventions);

• Nitrates for both preventing and for breakthrough chest pain
• Anti-platelet agents (e.g. aspirin and/or clopidogrel)
• Blood thinner (warfarin)
• B blockers (e.g. metoprolol, atenolol)
• ACE inhibitors or ARBs
• Cholesterol & triglycerides lowering agents
• High blood pressure therapy
• Diabetes mellitus therapy
• Lifestyle modification including
  • Smoking cessation
  • Exercise
  • Healthy diet etc.

Medications like beta blockers, ACE (angiotensin converting enzyme) inhibitors or ARBs (aldosterone receptor blockers) have been shown to improve the long term survival of patients with ischemic heart disease. They are now-a-days routinely used unless some contraindication exists.

Synopsis

Angina is like a warning symptom for the underlying serious heart condition; heed to this wake up call and get thoroughly evaluated by your doctor & implement their recommendations as early as possible to hopefully avoid encountering serious complications like heart attack.

Heart attack is one of the leading causes of death all over the world and the unhealthy lifestyle of modern era in the form of sedentary lifestyle & junk food has palpably contributed in this regard.

It is the result of sudden cessation or severe reduction in blood supply to an area of the heart muscle. Myocardial infarction (MI) is the medical term for this condition where myocardial means heart muscle related and infarction means damage to a tissue or organ caused by blockage of its blood supply.

Coronary artery disease (CAD) or ischemic heart disease (IHD) are other two terms commonly employed by medical personnel indicating the diseases of arteries supplying heart and the resultant angina (minor and reversible compromise of blood supply to the heart) or heart attack (severe and irreversible compromise of blood supply to the heart).

Risk factors

The following is a list of certain risk factors for the development of heart attack;

• High blood pressure (HTN)
• Diabetes mellitus (DM)
• Smoking
• High cholesterol (the bad cholesterol like LDL)
• Decreased good cholesterol (HDL)
• Elevated triglycerides
• History of heart disease in the family
• Increasing age
• Obesity
• Oral contraceptive pills (OCP) usage etc.

We do not have a control on certain risk factors like aging, family history etc but most other risk factors are under our control, at least to some extent,  like leading a healthy life style, adieu to smoking, sincere attempt to control medical conditions like HTN, DM etc.

How does heart attack develop or happen?

The heart attack is the result of severe and irreversible decreased blood supply to an area of heart muscle. The body cells are dependent on the arterial blood flow for their nutritional supply including the fuels like glucose for energy production, oxygen for various metabolic activities and myriad other nutrients to maintain the well being and functioning of the cells.

When there is especially a sudden cessation of arterial blood flow occurring, the body cells cannot sustain their normal functioning and if this continues for a critical amount of time the cell death takes place.

The blockage in an artery especially with the coronary arteries supplying the heart is mostly due to a condition called as atherosclerosis.  This is a gradual process developing over several years during which generally a progressive accumulation of cholesterol takes place on the inner margins of the arteries. Certain blood cells called as platelets and macrophages (cells like monocytes normally help in fighting infections) also take part in this process. This abnormal build up continues provided the patients do not do anything to halt it and a time may come when it starts compromising the blood supply in that artery. If it is partially occluding the artery then reversible or minor symptoms like angina occurs on the other hand if the blockage is complete it may result in the severe form, the heart attack.

Clinical Manifestations

Most often patients present with these symptoms;

• Chest pain
• Sweating
• Short of breath
• Sense of impending doom
• Symptoms of complications

Heart failure(short of breath, swelling of legs etc)
Cardiac arrhythmias (fainting, skipping of the heart beats etc)

The chest pain is described as constant squeezing or crushing feeling and usually located over left chest and breast bone area, some times radiating to the left arm, shoulder, neck etc. The severity and the discomfort are such that often patients require strong pain killers like morphine injection.

Diagnosis

Heart attack most often is a clinical diagnosis as patients will present with certain characteristic presentation. But some times they present with atypical manifestations, also there are a small percentage of patients that may not experience any symptoms at all (silent heart attack).

Irrespective of all these, certain investigations are always performed and such tests include;

• ECG
• Cardiac markers

Additional tests

• Echocardiogram
• Holter monitor
• Coronary angiogram
• Cardiac catheterization etc.

ECG and cardiac enzymes are the two most commonly employed tests and both can be accomplished easily in the emergency room where most of these patients land during an acute attack.

ECG records the electrical activities of the heart, and heart attack most often produces certain typical and diagnostic ECG changes. One of the most typical finding is what is called as “ST segment elevation”. ECG not only helps in confirming the diagnosis but also lets the doctor know how extensive is the damage and what area of the heart muscle is damaged etc.

Based on the ECG finding of ST elevation, whether present or not; MI is classified as ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI).

The cardiac markers usually checked include;

• Total CPK
• CPK-MB fraction
• Troponin etc.

Troponin is considered as the most sensitive and specific test for heart attack however total CPK & CPK-MB tests are also routinely performed.

Echocardiogram is an ultrasound technique for imaging the heart. This test may provide valuable clues regarding the global functioning of the heart including its wall motion, chamber size, valve function, blood flow, ejection fraction etc.

Cardiac catheterization & coronary angiograms are generally performed together. A catheter is passed through an artery like femoral artery and advanced to the aorta and a radioactive dye in injected such that it enters the coronary arteries and the radiological pictures are taken to look for any blockage. If required the catheter from the aorta is advanced to the left heart for additional evaluation. If right heart catheterization is required it is accomplished by passing the catheter through a vein like femoral vein.

Management

Stabilize the patient

Admit to a hospital.

Treatment of heart attack/MI pain:

• Nitrates (sublingual or intravenous)
• Inj morphine
• Beta blockers (e.g. injection metoprolol)

Acute therapies focusing the heart attack itself include (not all interventions required for every patent);

• Anti-platelet agents (e.g. aspirin and/or clopidogrel)
• Clot busters (reperfusion therapy);
  • tPA
  • Streptokinase
  • Urokinase
  • Reteplase etc.
• Primary PCI (Percutaneous Coronary Intervention);
  • Balloon angioplasty
  • Stent placement etc.
• CABG (coronary artery bypass grafting surgery)
• Blood thinners:
  • Low molecular weight heparins (e.g. enoxaparin)
  • Tab Warfarin
• ACE (angiotensin converting enzyme) inhibitors like lisinopril
• ARBs (angiotensin receptor blockers) like candesertan
• Hypotension/shock associated with heart attack
  • Inj Dobutamine
  • Inj Dopamine
  • Inj Milrinone

Long term therapy or preventive measures include;

• Anti platelet agents (reduce thickening of arteries)
• B blockers
• ACE inhibitors or ARBs
• Cholesterol, triglycerides lowering agents;
• High blood pressure therapy
• Diabetes mellitus therapy.
• Lifestyle modification including
  • Smoking cessation
  • Exercise
  • Healthy diet etc.

Medications like beta blockers, ACE inhibitors or ARBs have been shown to improve the long term survival of patients with heart attack. They are now-a-days routinely used unless some contraindication exists.

The NSTEMI treatment is generally approached in the similar lines as that of STEMI except the clot busters and PCI are not primarily used with NSTEMI.  Of course if sufficient indication exists then PCI can be performed in NSTEMI patients too.

Complications of heart attack

• Heart failure
• Cardiac arrhythmias
• Clot formation inside the heart chambers (with systemic embolism)
• Heart aneurysm
• Heart rupture
• Death

Female adults are the ones who usually develop varicose veins. It becomes more common in women as they age and usually has a familial predisposition. However, men may also develop varicosities but is usually not as noticeable because the varicosities are masked by their muscle mass. Those who work for prolonged periods while standing are also prone to developing varicosities. People who need to work while standing for long periods of time like doctors, nurses and sales clerks are all prone to developing varicosities. Pregnant women are also at risk for developing this because of the increased blood volume during pregnancy. Increased blood volume causes the veins to expand which can destroy the patency of the vessels. Varicose veins acquired during pregnancy usually do not regress completely but they may lessen after delivery of the fetus.

What Are The Symptoms?

The most common complaint among women is aesthetic. Mild cases do not usually have symptoms except that they do not like the unsightly veins on their legs. Moderate to severe cases will present with leg pain and leg heaviness which usually subsides with leg elevation. Some cases also present with itchiness, redness and skin dryness which is due to the reduced blood supply reaching that area.

How Is It Diagnosed?

It is can usually be diagnosed just by asking the history and performing a physical examination.

How Is It Treated?

There is no cure for the destroyed valves in varicose veins. However, there are procedures that can remove varicose veins. An old procedure involves the varicose veins being stripped off surgically but there are certain complications with this procedure including deep vein thrombosis, and pulmonary embolism.  Another option would be sclerotherapy in which veins are shrunk with the help of intravenous medications. Another popular procedure is Endovenous Laser Ablation which makes use of a laser to ligate varicose veins.

How Can It Be Prevented?

Varicose veins can be prevented minimizing physical inactivity. Staying too long in one position can facilitate pooling of blood in the lower extremity which can lead to varicosities. Physical exercise or even regular walks can stimulate good blood flow. If standing or sitting too long is required for work, the use of compression stockings is recommended. These special stockings compress the legs to prevent blood from pooling in the lower extremities. It can also be prevented by elevating the leg once in awhile.

Who Can Get It?
Anyone can develop hypertension but it is usually adults who develop hypertension due to atherosclerosis. Since atherosclerosis is caused by poor lifestyle practices like smoking, fatty diet and inactivity, adults are usually more at risk. It can also run in the family but it is not hereditary. A family history of hypertension only means that you are at an increased risk for developing hypertension but it can be prevented by staying away from other risk factors mentioned above.  Children and other adults can also develop hypertension but it may not be due to atherosclerosis. High blood pressure in children is usually due to other diseases such as kidney disease and other metabolic diseases.

What Are The Symptoms?
In adults, the usual symptoms include headache at the nape area, light-headedness and blurring of vision. However, some patients may not even feel anything at all. Hypertensive patients who don’t experience symptoms are more at risk of developing complications because health-seeking behavior is delayed.

How Is It Diagnosed?
High blood pressure can be detected using a sphygmomanometer. However, a diagnosis of hypertension is only made after measuring high blood pressure on 3 different occasions. The diagnosis of hypertension is usually classified further into 3 stages: Pre-hypertensive, Stage 1 Hypertension and Stage 2 Hypertension. Pre-hypertensive blood pressure is 120-139/80-89 mmHg, Stage 1 Hypertension is 140-159/90-99 mmHg while Hypertension Stage 2 is 160/100 mmHg and above. The antihypertensive medications that the physician will prescribe will depend on the stage. Combination drugs like diuretics, calcium blockers and beta blockers are usually required when stage 2 is reached.

How Is It Treated?
There is no cure for hypertension but it can be controlled to prevent complications.The antihypertensive medications that the physician will prescribe will depend on the stage of hypertension. Usually, 1 type of drug such as diuretics or calcium blockers will suffice for Stage 1 hypertension. However, various drugs are usually combined in Stage 2 hypertension such as diuretic combined with Angiotensin Receptor Blockers, Calcium blockers, ACE inhibitors or Beta blockers.

How Is It Prevented?
Hypertension can be prevented by maintaining a healthy lifestyle as early as possible. Regular exercise can prevent obesity which can put you at risk for hypertension. A healthy diet high in fiber and low in fat and cholesterol can also lessen the risk for hypertension. Smoking is also an important risk factor for developing hypertension and other serious diseases such as lung cancer and emphysema that is why it should be avoided at all costs.