50 cases in clinical cardiology pdf free download

50 cases in clinical cardiology pdf free download

This patient was operated upon for a cardiac defect, when she was 3 years old. The most common congenital cyanotic heart disease that is associated with survival until adolescence and sometimes even into adulthood is tetralogy of Fallot.

The right ventricular enlargement that ensued, led to secondary tricuspid regurgitation because of annular dilatation. Tetralogy of Fallot is the most common congenital cyanotic heart disease that survives into adolescence. It is associated with a right-to-left shunt since birth unlike isolated septal defects which are left-to-right shunts and undergo reversal only after the development of pulmonary hypertension.

The four components Fig. Rarely, the pulmonary valve is absent pulmonary atresia. The ventricular septal defect VSD is membranous in location. The aorta is displaced rightward and overrides the septum, the overriding aorta OA. Therefore, the septum is not in line with the anterior aortic wall but with the aortic valve closure point.

Rarely, an atrial septal defect ASD may be associated, in which case the constellation is designated as pentalogy of Fallot. The S2 is single because the P2 is muffled and the A2 is loud because the aorta is anteriorly placed. The systolic murmur originates from the subvalvular pulmonary stenosis and not from the ventricular septal defect.

Congestive heart failure is rare because the septal defect balances the right and left ventricular pressures. If left unrepaired, catastrophic complications in adolescence are arterial thrombo-embolism and cerebral abscess. These shunt procedures were performed to bypass the RVOT obstruction and to enhance pulmonary blood flow. These shunts were Blalock-Taussig shunt subclavian artery to pulmonary artery and Waterston shunt ascending aorta to right pulmonary artery.

However, even after these procedures, patients remained symptomatic and complications occurred unabated. Nowadays, total surgical correction is undertaken to close the shunt and to enhance pulmonary blood flow. This includes patch closure of the VSD with pulmonary subvalvular muscle resection and valvotomy. Cardiac surgeons are increasingly encountering complications of prior surgical correction, as these children survive into their teens.

Complications after surgery include residual shunt, residual stenosis or, post-valvotomy pulmonary regurgitation and right ventricular enlargement as in our case. Pulmonary valve replacement with tricuspid annular repair would be the best course of action in this case.

Modern cardiac imaging techniques of computed tomography CT and magnetic resonance imaging MRI are particularly useful to evaluate postoperative patients.

Pulmonary balloon angioplasty and artificial valve deployment by non-surgical intervention have been recently described. The episodes of palpitation were associated with some light-headedness, but she had never fainted. Her palpitation was at times related to some emotional upset or undue physical exercise, but there was no history of exertional fatigue, chest pain or breathlessness.

There was also no history of tremor of the hands or weight loss. Her childhood had been uneventful with normal growth milestones and there was no history of cyanotic spells during sports activities. She also denied having had recurrent sore- throat, joint pains or any prolonged febrile illness during her school days.

On examination, the patient was comfortable, relaxed and not dyspneic. The JVP was raised 5 cm above the angle of Louis and showed large v waves with a prominent y descent. On examining the abdomen, there were visible epigastric pulsations, with the liver edge 6 cm below the right costal margin and pulsatile; no ascites was demonstrable. The apex beat was normal in nature and location but a left parasternal heave was palpated.

The S1 and S2 were both split with wide splitting of S2 appreciated during inspiration. No S3 or S4 gallop sound was heard. A pansystolic murmur was audible at the lower end of the left sternal edge. Breathing was vesicular and no rhonchi or crepts were heard over the lung fields.

ECG showed tall P waves P. X-ray chest finding was an enlarged cardiac silhouette, more so towards the right of the midline. ECHO revealed normal sized left ventricle with normal ejection fraction. The mitral and aortic valves were normal and the left atrium was not dilated.

There was no echo drop-out in the region of either septum. However, the right atrium was markedly enlarged and the right ventricle was dilated as well as hyperkinetic. On colour flow mapping, a regurgitant jet was seen in the right atrium. In a young woman, history of episodic palpitation raises several clinical possibilities.

Anxiety neurosis, panic attacks and paroxysmal supraventricular tachycardia are usual causes but in these, the heart is structurally normal. Perimenopausal symptoms in women include palpitation but our patient was young. Mitral valve prolapse MVP and atrial septal defect ASD are structural cardiac abnormalities that are responsible for tachyarrhythmias. However, in our case the mitral valve was normal and there was no septal defect.

The physical examination of the patient and interpretation of simple cardiac investigations is a good exercise in bed-side clinical cardiology. A raised JVP with large v waves and prominent y descent are characteristic of tricuspid regurgitation into the right atrium Fig.

So is an enlarged and pulsatile liver on abdominal examination. A sustained left parasternal heave is indicative of right ventricular volume overload. Figure 4. Sometimes, the S2 is single because of soft P2 due to low pulmonary ejection volume. The pansystolic murmur of tricuspid regurgitation is best audible over the lower left parasternal area and does not radiate towards the axilla or the base of the heart.

At times, the rhythm is atrial fibrillation. On X-ray chest, the cardiac silhouette is enlarged towards the right of the midline, due to the large right atrium Fig. Superficially, this resembles a pericardial effusion. The differentiating feature is that the right lower portion of the cardiac silhouette curves inwards towards the center of the chest and not outwards, as it would in case of pericardial effusion. On ECHO apical view, there is downward displacement of the tricuspid valve into the body of the right ventricle, towards the apex.

The septal tricuspid Figure 4. The tricuspid leaflet is large and shows wide excursion, often with a whip-like motion. The right ventricle is dilated and hyperkinetic due to volume overload. On long-axis view, because of downward displacement of the tricuspid valve, there is simultaneous recording of the mitral and tricuspid valves MV and TV.

The commonest reason for tricuspid regurgitation is dilatation of the tricuspid valve annulus secondary to right ventricular dilatation. Reason for annular dilatation is usually pulmonary hypertension due to congenital left-to-right shunt, rheumatic mitral valve disease or chronic cor pulmonale.

Sometimes, dilated cardiomyopathy causes annular dilatation Table 4. Primary tricuspid valvular regurgitation has several causes except coronary artery disease and systemic hypertension, the commonest forms of heart disease. Table 4. Drugs that block the atrioventricular AV node to reduce the heart rate, such as betablockers and verapamil, are the agents of choice. In the presence of WPW syndrome, amiodarone is preferable.

Digoxin may be used to treat atrial fibrillation in which case, an anticoagulant is also prescribed to reduce the risk of thrombo-embolism. If the tachyarrhythmias are refractory to drug treatment or an accessory bypass tract is present, radiofrequency ablation can be offered.

In the presence of moderate to severe tricuspid regurgitation, valve repair with restrictive annuloplasty or even valve replacement may be considered. While auscultating the chest of the child, the pediatrician incidentally heard a loud murmur over the upper precordium.

Although the child had been taken to several doctors in the past for consultation and vaccination, nobody had noticed the murmur. The boy was born after normal vaginal delivery, without any intervention and was not cyanosed at birth.

His mother had experienced no difficulty in nursing him. On examination, the child was irritable because of his respiratory catarrhe but not tachypneic. He was febrile but not anemic or icteric and there was no cyanosis or clubbing of the fingers or toes.

The thyroid gland was not enlarged and there was no sign of congestive heart failure. On examination of the precordium, the apex beat was hyperkinetic but there was no palpable parasternal heave. The loud murmur over the precordium was wide-spread but maximally audible in the 2nd left intercostal space, just below the middle of the left clavicle. On careful auscultation, the murmur was pansystolic but extended upto and through S2, well into diastole.

No S3 or S4 sound could be appreciated because of the long murmur. The lung fields were clear on auscultation without any rhonchi or crepitations. A good volume radial pulse, which can be appreciated even with the arm elevated above the head, is known as collapsing pulse. A collapsing pulse is indicative of a wide pulse pressure. A long murmur that extends throughout systole and crosses S2 to spill over into diastole, is known as a continuous murmur.

X-ray chest findings were cardiomegaly with left ventricular contour and a prominent main pulmonary artery with pulmonary plethora Fig. On ECHO, the left ventricle was dilated with normal systolic function. The left atrium was also dilated and all cardiac valves were structurally normal. On colour flow mapping, there was a retrograde mosaic jet extending from the left pulmonary artery to the dilated main pulmonary artery Fig.

Figure 5. The estimated pulmonary artery pressure was normal. Therefore, the definite diagnosis in this case is patent ductus arteriosus. The ductus arteriosus is a channel that connects the descending aorta distal to the origin of left subclavian artery, to the left pulmonary artery just distal to the bifurcation of main pulmonary artery. The ductus remains open during intrauterine life and closes soon after birth when its purpose is fulfilled. When the ductus fails to close physiologically within 24 hours after birth and anatomically within a week, it provides a communication between the aortic and pulmonary circulations.

Flow from the aorta at higher pressure to the pulmonary artery at lower pressure creates a left-to-right shunt across the PDA Fig. Persistence of the ductus is sometimes associated with maternal rubella syndrome and premature delivery. It is maximally audible below the middle of the left clavicle, just before and just after the S2.

The continuous murmur may be accompanied by a mid-diastolic murmur over the mitral area, due to torrential flow across the mitral valve. There may also be reverse splitting of S2, due to delayed closure of the aortic valve. When pulmonary hypertension develops, the murmur of PDA is confined to systole. As already mentioned, there are several causes of a continuous murmur. In aorto-pulmonary window, there is a proximal communication between the aorta and the pulmonary artery.

Although the murmur of aortic coarctation is typically systolic, in tight stenosis the murmur may extend into diastole. Venous hum is a low-pitched continuous murmur which is loudest over the supraclavicular fossa, but sometimes also heard over the precordium.

It is accentuated by looking over the shoulder while sitting and abolished by compression of the jugular vein. It is better appreciated while lying down and during systole. Coronary fistula and ruptured aneurysm of sinus of Valsalva are rare arterio-venous communications that can also produce a continuous murmur. Ventricular septal defect VSD produces a pansystolic murmur while aortic regurgitation causes an early diastolic murmur. When the two are associated as in perimembranous VSD, the murmur is systolo-diastolic.

A similar systolo- diastolic murmur occurs when an atrial septal defect ASD is associated with mitral stenosis, the Lutembacher syndrome. In contrast to a continuous murmur, the two components of a systolo-diastolic murmur have a different character. PDA is the commonest cause of cardiomegaly and heart failure in infancy and childhood.

Conversely, heart failure is the commonest cause of morbidity and mortality in PDA, at any age. When pulmonary hypertension develops in PDA, reversal of the shunt from pulmonary artery to aorta may occur. In that case, the continuous murmur gets shorter and quieter. The toes get more cyanosed and clubbed than the fingers. The reason for this differential cyanosis is that the ductus is distal to the left subclavian artery and predominantly the lower limbs get deoxygenated blood.

Other complication of PDA are endarteritis, aneurysm formation and rarely rupture of the ductus. All PDAs of significant size and shunt should be ligated, except in ductus dependent complex congenital cyanotic heart diseases of infancy.

She denied any chest pain, wheezing or hemoptysis. At the age of 12, she had a prolonged febrile illness with joint pains and ever since, she had been receiving monthly injections of penicillin. On examination she was tachypneic with pallor but there was no cyanosis or icterus.

Her temperature was F. The JVP was not raised, thyroid gland was not enlarged and there were no palpable lymph nodes. There was no evidence of pharyngo-tonsillitis, swollen joints or petechial spots over the skin, eyes or finger-tips. The apex beat was tapping in nature with a left parasternal heave. The S1 was loud and the P2 was also accentuated. A low-pitched mid-diastolic rumbling murmur was heard over the cardiac apex.

The murmur was preceded by an opening snap and accentuated just before systole. There were scattered rhonchi and crepts over the lung fields. The S1 is loud Figure 6. Other reasons for a loud S1 are sinus tachycardia and a short P-R interval, where the diastole is short. The mid-diastolic murmur of mitral stenosis MS is best heard with the patient in the left lateral decubitus position, using the stethoscope bell.

The length of the murmur correlates with the severity of stenosis. The murmur undergoes presystolic accentuation due to atrial contribution to ventricular filling. In mild MS, the murmur may be only presystolic. If MS is associated with atrial fibrillation the S1 is variable in intensity due to variable duration of diastole.

Also, presystolic accentuation is lost due to lack of atrial contribution to ventricular filling. Presystolic accentuation is also absent in a calcified valve and after commissurotomy. Severe mitral stenosis may be silent due to low cardiac output and the fact that the right ventricle underlies most of the precordium because of clockwise cardiac rotation.

The opening snap heralds the onset of ventricular diastolic filling and the end of isovolumic relaxation. It indicates pliability of the valve, suitability for valvotomy and is absent in a heavily calcified valve or after commissurotomy.

Besides mitral stenosis, other reasons for a mid- diastolic murmur are acute rheumatic valvulitis Carey-Coomb murmur , aortic regurgitation Austin-Flint murmur , left atrial myxoma prolapse into mitral orifice and left-to-right shunt increased transmitral inflow. Figure 6. X-ray chest findings were straightening of the left heart border with pulmonary congestion. On M-mode ECHO, excursion of the anterior leaflet was reduced with paradoxical excursion of the posterior leaflet Fig.

The mitral valve leaflets were thickened with limited excursion and restricted valve opening. The anterior mitral leaflet showed diastolic doming Fig. There was no abnormality of the aortic valve and the estimated pulmonary artery pressure was elevated. The severity of mitral stenosis can be gauged and classified, according to several calculated indices from echocardiography. The peak velocity and pressure gradient depend on the heart rate and stroke volume.

Measurement of mitral valve area may be fallacious due to heavily calcified leaflets, subvalvular pathology and prior commissurotomy.

Rheumatic heart disease is the predominant cause of mitral stenosis. Complications of MS are pulmonary congestion, respiratory infections, hemoptysis, right heart failure and systemic thrombo-embolism due to atrial fibrillation associated with left atrial thrombus. Table 6. Throat-swab culture for beta- hemolytic Streptococcus and bacterial blood cultures may be included.

Transthoracic ECHO is central to the diagnosis and assessment of mitral stenosis. Besides determining the severity of MS, it can assess left atrial size, left ventricular function and estimate pulmonary artery pressure.

Transesophageal echocardiography TEE allows better assessment of the subvalvular and commissural architecture and improves the detection of a left atrial thrombus. Diuretics reduce pulmonary congestion, especially in patients with associated mitral or aortic regurgitation. Rate control with digoxin, beta-blocker or verapamil improves left ventricular diastolic filling, in patients who are in sinus rhythm and controls the ventricular response, in whom the rhythm is atrial fibrillation.

Since atrial fibrillation in patients with mitral stenosis is associated with a high risk of thrombo-embolism, these patients should also be on a long-term oral anticoagulant agent like warfarin. Recurrence of symptoms after valvotomy is more often due to induced mitral regurgitation rather than restenosis. If valvotomy cannot be performed because of the aforementioned reasons, mitral valve replacement MVR is undertaken.

During MVR, if atrial fibrillation is present, left atrial radiofrequency ablation RFA and appendage ligation are also performed. She complained of exertional shortness of breath and had a cardiac murmur. She was a known case of hypertension, adequately controlled by medication. Her breathlessness had been felt since the last 4 months but had significantly worsened over the preceding 2 weeks.

There was no history of exertional chest pain or of palpitation and fainting. She did not smoke or consume alcohol but she seldom exercised and did not follow the diet-plan suggested by her physician. On examination, she was overweight without any clinical signs of cortisol excess or hypothyroidism. There was no sign of heart failure. The apex beat was hyperdynamic, ill-sustained heaving in nature and displaced towards the left axilla.

The S1 was soft. A2 was loud and a soft S3 was audible in early diastole. A soft blowing pansystolic murmur was audible over the mitral area, that radiated towards the axilla. Also, a short diastolic rumble was heard over the cardiac apex. Few basilar rales were auscultated over the lower lung fields. Figure 7. The S1 was soft since the mitral leaflets are close to each other at the end of diastole and snap together softly. The A2 was loud due to associated systemic hypertension. The displacement of the apex beat and audible S3 sound are indicative of left ventricular diastolic overload.

The S3 is a low-pitched sound that follows the A2. It indicates abrupt halting of left ventricular filling. Physiological S3 is appreciated in mitral regurgitation, left-to-right shunt and high cardiac output states. Pathological S3 is audible in aortic regurgitation and left ventricular systolic dysfunction. The pansystolic murmur of mitral regurgitation typically radiates to the left axilla and sometimes even to the left scapula , if the anterior mitral leaflet is diseased. It radiates to the base of the heart, if the posterior mitral leaflet is involved.

This differentiates it from the pansystolic murmur of tricuspid regurgitation or a ventricular septal defect. The accompanying diastolic rumble does not necessarily indicate concomitant mitral stenosis and is due to torrential flow across the valve, which is the sum of normal atrial blood volume and the regurgitant volume. It is worth mentioning that the murmur of acute or severe MR is not pansystolic but early systolic, because less turbulence is generated by the large valve orifice.

Moreover, the rapid rise of left atrial pressure impedes regurgitation during later systole. The murmur of mitral annular calcification is also typically early systolic. X-ray chest findings were moderate cardiomegaly, pulmonary congestion and straightening of the left heart border Fig.

In acute MR due to ruptured chordae tendinae, there is minimal left ventricular dilatation. The mitral valve leaflets were thickened and fibrotic indicating rheumatic MR. Other potential abnormalities of the mitral valve in case of MR are mitral leaflet redundancy and prolapse, flail leaflet, annular calcification or vegetations in case of endocarditis. However, there are some fallacies associated with these calculations. The spatial profile of the MR jet does not truly reflect the regurgitant volume.

It depends upon the shape of the valve orifice, the angle of the jet, left ventricular filling pressure and the size of the left atrium. Table 7. Usual causes of primary MR are rheumatic heart disease, mitral leaflet prolapse, papillary muscle dysfunction, infective endocarditis and mitral annular calcification.

Occasionally, secondary MR is due to mitral annular dilatation, as a result of dilated or ischemic cardiomyopathy. Acute MR can result from rupture of papillary muscle or chordae tendinae in case of myocardial infarction, infective endocarditis or after blunt trauma to the chest Table 7.

Those undergoing a dental or surgical procedure, need antibiotic prophylaxis against infective endocarditis. Vasodilators such as ACE inhibitors or ARBs combined with a diuretic relieve pulmonary congestion, especially if systemic hypertension is present.

Digoxin and an anticoagulant are used if there is concomitant atrial fibrillation. Secondary MR is reduced by lowering preload and afterload, which decrease the diameter of the mitral annulus. Surgical operations for MR are mitral valve repair and valve replacement. Repair of the valve or annuloplasty is preferable if the valvular anatomy is suitable, since it preserves left ventricular geometry and spares the patient from the problems of anticoagulation. Replacement of the valve is indicated if the valvular anatomy is severely distorted.

The MR is not due to an intrinsic valvular abnormality, but the result of ventricular dilatation with annular enlargement, papillary muscle dysfunction and dysfunctional ventricular remodeling with increased sphericity. These patients can be offered restrictive annuloplasty, which involves insertion of an undersized annular ring to improve leaflet apposition. Therefore, patients who are to undergo coronary artery bypass graft CABG surgery should be adequately assessed preoperatively for mitral regurgitation.

The chest pain was precordial in location and described as sharp and pricking. There was no feeling of tightness in the chest or suffocation and the pain did not radiate to the left arm or lower jaw. The episodes of chest pain and palpitation were unrelated to physical exercise, taking meals or change in body posture, but usually related to some emotional upheaval.

She had first experienced these symptoms during her final high-school exams at the age of 18, but the frequency of episodes had significantly increased, ever since her arranged marriage 3 months back.

There was history of repeated sore-throat during childhood, but she never had a prolonged febrile illness with painful joints. On examination, the patient had a slender body habitus with an anxious look on her face. The extremities were warm with sweaty palms and a fine distal tremor.

There was no anemia, cyanosis or edema and the JVP was not raised. The precordium was hyperdynamic with a pectus excavatum sternal deformity. The apex beat was normal in location and there was no parasternal heave. The S1 was loud, S2 was normally split and no S3 or S4 was heard in diastole. A high-pitched systolic murmur was audible between the cardiac apex and the left sternal border.

The murmur started well after the S1 and had a typical honking character. It was associated with a sharp clicking sound in mid-systole. The most likely diagnosis in this case is mitral valve prolapse MVP. The mid-systolic click is a high-pitched sharp sound produced by sudden tensing of the redundant mitral leaflet.

At times, multiple clicks are appreciated. This is often followed by a mid- or late-systolic murmur that typically has a whooping or honking character. The click and murmur can vary with alteration of left ventricular LV volume, by change in patient posture. During standing or Valsalva manoeuvre, when the LV volume is reduced, the click moves closer to S1 and the murmur becomes louder.

Conversely, during squatting when the LV volume increases, the click moves closer to S2 and the murmur becomes softer.

In mitral valve prolapse syndrome, the SI is loud for several reasons. The high adrenergic activity increases the heart rate and shortens diastole. The wide excursion of the myxomatous, redundant valve leaflet increases the force of mitral valve closure. Finally, merger of the non-ejection click with the S1 , increases the intensity of the latter. Figure 8.

The X-ray chest was unremarkable. On ECHO, the left ventricle was normal in size and systolic function, but the left atrium was mildly dilated. The anterior mitral leaflet was thick and redundant, with systolic buckling above the plane of the mitral annulus into the left atrium Fig. On colour flow mapping, an eccentric regurgitant jet was seen entering the left atrium.

In type 1, the anterior leaflet only moves upto the annulus while in type 2, it bows into the left atrium. In type 3, both the leaflets enter the left atrium. Strict echocardiographic criteria must be used to diagnose MVP because needless anxiety may be created by over-reporting this abnormality. Conversely, true MVP may be missed due to low transducer position and cranial angulation. Table 8. Often these women have a type A personality with history of panic attacks and migranous headaches.

They may have a slender body habitus with thoracic skeletal deformities including pectus excavatum, straight back and scoliosis. The valvular abnormality is due to myxomatous degeneration leading to thickening, nodularity or redundancy of one or both mitral leaflets. Mitral regurgitation may be present due to faulty coaptation of leaflets and predisposes to endocarditis. Whether these non-specific symptoms are directly attributable to MVP or due to autonomic dysfunction, continues to be widely debated and their cause- effect relationship remains unproven.

Besides the classical symptoms, focal neurologic findings, such as transient ischemic attacks, amaurosis fugax, retinal artery occlusion and rarely hemiparesis have all been reported in patients with MVP.

These neurologic findings probably occur as a result of thrombo-embolism from the prolapsing valve. Premature beats are most common, although practically any arrhythmia can occur. The cause of the arrhythmia is not known but may be related to autonomic dysfunction or mechanical effects of the floppy valve. Incidence of syncope correlates poorly with the presence of arrhythmias. Ambulatory hour Holter monitoring frequently shows supraventricular and sometimes ventricular ectopic beats and rarely if ever reveals life-threatening arrhythmias.

Myocardial perfusion imaging and coronary angiography expectedly do not show any significant abnormality. Hormonal assays are sometimes performed to rule out thyrotoxicosis and likewise, urinary catecholamines are rarely measured, to rule out the possibility of phaeochromocytoma. Anxiolytic drugs during the day with a mild tranquilizer at night are useful for those having overt anxiety and disturbed sleep. A beta-blocker such as propranolol has multiple benefits in these patients.

It controls tachycardia and ectopic beats, reduces the degree of leaflet prolapse, treats the associated tremor and serves as a prophylactic drug against migraine. Low-dose aspirin is prescribed to prevent thrombo-embolism. Patients of MVP with mitral regurgitation MR and not those without demonstrable MR, require antibiotic prophylaxis against infective endocarditis, prior to a dental, endoscopic or surgical procedure.

In the preceding month, he had experienced three distinct episodes of dizziness, followed by fainting. The syncopal episodes were unrelated to exercise and were not preceded by palpitation or chest pain. There was no history of prolonged febrile illness or joint pains during childhood.

There was no anemia, cyanosis or icterus and the thyroid gland was not enlarged. The JVP was not raised and there was no ankle edema. The apex beat was normal in position and heaving in nature. The S1 was normal, S2 appeared single and S4 was audible in pre-systole. An ejection systolic murmur was audible over the aortic area, that was preceded by an ejection click and associated with a palpable thrill.

The murmur and thrill typically radiated towards the carotid arteries. The most likely diagnosis in this case is aortic valve stenosis Fig. A pulse of low volume pulsus parvus with slow upstroke pulsus tardus is a typical feature of aortic valve stenosis.

A heaving apex beat indicates left ventricular hypertrophy and is also observed in uncontrolled systemic hypertension and in coarctation of aorta. The low-pitched S4 sound in pre-systole, indicates forceful atrial contraction over a non-compliant left ventricle. It coincides with the a wave of the jugular vein. The S4 is always pathological in aortic stenosis, systemic hypertension and restrictive or hypertrophic cardiomyopathy.

An acute rise in left ventricular end- diastolic pressure LVEDP as in acute coronary syndrome or acute valvular regurgitation causes acute onset of S4. The S2 appears single because the A2 is muffled. If A2 is audible, the splitting of S2 is paradoxical or reverse, with the A2 following the P2 due to prolonged left ventricular ejection time.

The ejection click heralds the onset of systole and the end of isovolumic relaxation. The click may be absent if the valve is heavily calcified. The ejection systolic murmur of aortic stenosis indicates turbulent flow across the narrow aortic valve orifice.

It is described as a diamond- shaped murmur, since it builds up and declines gradually, with maximal intensity in mid-systole. This pattern coincides with the temporal profile of the pressure gradient across the valve. Length and loudness of the murmur does not correlate with the severity of aortic stenosis. Figure 9. X-ray chest findings were a boot-shaped heart with a prominent ascending aorta, suggestive of post- stenotic dilatation. On ECHO, the left ventricular cavity was small in size, with a good ejection fraction.

The aortic valve leaflets were thickened and calcific with restricted excursion and reduced opening of the valve. Due to fusion at the leaflet tips, there was systolic doming of leaflets. On colour flow mapping, a mosaic jet was observed in the proximal aorta Fig. However, the severity of stenosis is determined from the peak velocity and pressure gradient across the valve on Doppler Table 9.

Measurements from various echo views are taken to obtain the peak aortic flow velocity. In rheumatic aortic stenosis, assessment of concomitant mitral valve abnormalities is crucial as the mitral valve is almost invariably involved. Finally, left ventricular wall thickness, end-diastolic diameter and ejection fraction are to be measured. There are some fallacies associated with the calculation of aortic stenosis severity.

Reverberation artifacts in a heavily calcified valve may overestimate AS severity. They also depend upon the degree of parallelism obtained between the Doppler beam and aortic flow direction. Table 9. Congenital bicuspid aortic valve leads to aortic stenosis because of increased mechanical and shear stress on the valve and usually presents in the 4th of 5th decade. Calcific aortic stenosis is akin to atherosclerosis and accompanied by multiple cardiovascular risk factors.

It typically presents in the 6th or 7th decade of life. Rarely, a discrete membrane or ring may cause subvalvular or supravalvular AS. Complications of AS are left ventricular hypertrophy with diastolic dysfunction earlier on and systolic heart failure in the later stages.

Syncopal episodes are due to tachyarrhythmias or LVOT obstruction. Angina may occur because of coronary ostial stenosis or the increased oxygen demand of the hypertrophied myocardium.

The characteristic response is a drop in blood pressure during the test due to vasodilatation and failure of the cardiac output to rise. Patients with a positive test may be taken up for valve replacement. Coronary angiography is indicated to assess the coronary circulation and need by bypass graft surgery CABG , at the time of aortic valve replacement. Besides showing occlusive coronary disease, angiography may reveal coronary ostial stenosis due to calcification of the aortic valve.

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