Kelainan Katup Jantung

Aortic Stenosis (AS)

Aortic Regurgitation (AR)

Mitral Stenosis (MS)

Mitral Regurgitation (MR)

Mitral Valve Prolapse (MVP)

Tricuspid Regurgitation (TR)

01Pathophysiology

Stenotic Lesions

Valve stenosis creates a pressure overload on the chamber proximal to the obstruction. The heart compensates through concentric hypertrophy, in which the wall thickens to normalize wall stress according to the law of Laplace ($\text{Wall stress}=\frac{P\times r}{2h}\backslash text\{Wall\; stress\}\; =\; \backslash frac\{P\; \backslash times\; r\}\{2h\}$, where $PP$ is pressure, $rr$ is radius, and $hh$ is wall thickness).

In aortic stenosis, the left ventricle faces progressively increasing resistance to ejection. The LV wall thickens concentrically, maintaining stroke volume at rest for years. However, this thick, stiff ventricle has impaired diastolic relaxation and becomes increasingly dependent on atrial contraction for filling. This is why atrial fibrillation is so poorly tolerated in AS: loss of the "atrial kick" can precipitate acute heart failure. The classic triad of symptoms (syncope, angina, dyspnea) maps directly to the pathophysiology. Syncope occurs because the fixed obstruction prevents adequate cardiac output augmentation during exertion. Angina results from a supply-demand mismatch: the hypertrophied ventricle has increased oxygen demand, but elevated intramural pressures compress the subendocardial coronary vessels, reducing supply. Dyspnea reflects diastolic dysfunction and eventual systolic failure.

In mitral stenosis, the obstruction sits at the level of the mitral valve, causing left atrial pressure to rise. The left atrium dilates over time, which has two important consequences. First, atrial dilation predisposes to atrial fibrillation, the most common complication. Second, elevated left atrial pressure transmits backward to the pulmonary vasculature, causing pulmonary hypertension, pulmonary edema, and eventually right heart failure. The left ventricle itself is typically normal in size and function because the problem is upstream of it. This is a commonly tested point: if a vignette shows a dilated LV in the context of mitral stenosis, reconsider the diagnosis.

Regurgitant Lesions

Valve regurgitation creates a volume overload on the receiving chamber. The heart compensates through eccentric hypertrophy, in which the chamber dilates and sarcomeres are added in series.

In aortic regurgitation, blood leaks back into the LV during diastole, increasing preload. In chronic AR, the LV gradually dilates to accommodate the extra volume, and total stroke volume increases (forward flow + regurgitant volume). This produces the widened pulse pressure: systolic pressure is high because the heart ejects a large volume, and diastolic pressure is low because blood runs off back into the LV. All of the classic exam findings (bounding pulses, head bobbing, nail-bed pulsations) are manifestations of this wide pulse pressure. In acute AR, the LV has no time to adapt. The sudden regurgitant volume floods a normal-sized, noncompliant ventricle, causing an abrupt rise in LV end-diastolic pressure that transmits to the left atrium and pulmonary vasculature, resulting in acute pulmonary edema. This distinction between chronic and acute AR is a favorite testing point.

In mitral regurgitation, blood leaks backward into the left atrium during systole. In chronic MR, the left atrium dilates to accommodate the extra volume, blunting the rise in atrial pressure. Patients may remain compensated for years. In acute MR (papillary muscle rupture after MI, chordal rupture), a normal-sized, noncompliant left atrium cannot accommodate the sudden regurgitant volume. Atrial pressure rises sharply, producing flash pulmonary edema. This is a classic post-MI complication question: a patient who was recovering from an MI suddenly develops severe pulmonary edema and a new murmur. Think papillary muscle rupture.

In mitral valve prolapse, the myxomatous degeneration allows the mitral leaflets to billow into the left atrium during systole. The mid-systolic click is produced when the redundant leaflet tissue reaches maximum excursion and the chordae tendineae snap taut. If the prolapse is severe enough, the leaflets fail to coapt and a late systolic murmur of MR follows the click. The key concept for the exam is how LV volume affects the click timing. When LV volume is smaller (standing, Valsalva, dehydration), the valve reaches its prolapse point sooner, and the click and murmur occur earlier in systole and the murmur becomes longer. When LV volume is larger (squatting, leg elevation), the click is delayed and the murmur shortens.

In tricuspid regurgitation, right-sided volume overload produces the classic findings of right heart failure: JVD, peripheral edema, hepatomegaly, and ascites. The pulsatile liver occurs because the regurgitant systolic wave transmits through the hepatic veins into the liver parenchyma. The Carvallo sign (murmur louder with inspiration) distinguishes right-sided murmurs from left-sided murmurs: inspiration increases venous return to the right heart, augmenting the regurgitant volume and intensifying the murmur.

02Classification and Clinical Manifestation

Murmur Classification by Timing and Mechanism

Severity Grading of Common Lesions

Dynamic Auscultation: The Master Table

This table is one of the highest-yield topics in all of cardiology for the exam. Understanding maneuvers will appear in multiple questions.

The critical insight: most murmurs get louder with increased preload and afterload. The two exceptions are MVP and HOCM, which get louder with decreased LV volume. This is the single most commonly tested concept regarding murmurs.

03Diagnostic Workup

Echocardiography is the cornerstone of all valvular heart disease evaluation. For the exam, if a question presents a patient with a murmur and asks "what is the next best step," the answer is virtually always transthoracic echocardiography (TTE). TTE serves as both the best initial test and the most accurate test for nearly every valve lesion. It provides real-time assessment of valve morphology, chamber sizes, pressure gradients, regurgitant volumes, and ventricular function.

Transesophageal echocardiography (TEE) offers superior imaging quality because the probe sits directly behind the heart in the esophagus, eliminating chest wall and lung interference. TEE is ordered when TTE images are inadequate, when endocarditis is suspected (to look for vegetations), and during preoperative planning to define valve anatomy before repair.

Cardiac catheterization is reserved for situations where noninvasive imaging is inconclusive or when there is a discrepancy between clinical findings and echocardiographic data. In aortic stenosis, if echocardiography shows low gradient but low ejection fraction (low-flow, low-gradient AS), a dobutamine stress echocardiogram can help distinguish true severe AS from pseudo-severe AS. Catheterization can also directly measure transvalvular gradients.

A few diagnosis-confirming findings worth memorizing:

• Aortic stenosis: The closer the opening snap of the S2-OS interval (in cases with calcified valves, S2 may actually be absent or single), the more severe. In AS, a paradoxically split S2 (A2 delayed past P2) can occur because prolonged LV ejection delays aortic valve closure. A single S2 or absent A2 suggests severe calcification with an immobile valve.

• Mitral stenosis: The shorter the S2 to opening snap interval, the more severe the stenosis (higher LA pressure forces the valve open sooner). This is a classic board question.

• Aortic regurgitation: Look for a wide pulse pressure on vitals and echocardiographic evidence of diastolic flow reversal in the descending aorta (a sign of severe AR).

ECG findings serve as supporting evidence but are never the primary diagnostic modality. Look for LVH patterns in left-sided valve disease and right axis deviation or RVH in conditions causing right heart strain (e.g., severe MS leading to pulmonary hypertension).

Chest X-ray findings that point to valvular disease include: calcification of the aortic valve (AS), cardiomegaly (chronic regurgitant lesions), left atrial enlargement visible as straightening of the left heart border and a double density behind the cardiac silhouette (MS), and pulmonary vascular congestion (any decompensated valve disease).

04Management and Treatment

Aortic Stenosis

There is no effective medical therapy that slows the progression of aortic stenosis. Statins do not reduce valve calcification or delay the need for surgery (this was disproven in clinical trials and is a frequent distractor). The cornerstone of management is monitoring with serial echocardiography until the patient becomes symptomatic or meets criteria for intervention.

Once symptoms develop, prognosis without surgery is dismal: mean survival is 5 years with angina, 3 years with syncope, and 2 years with heart failure. This is worth memorizing because questions will ask about the natural history.

SAVR (surgical aortic valve replacement) is the standard intervention for low-to-intermediate risk patients. TAVR has emerged as the preferred option for patients at high or prohibitive surgical risk and is increasingly used in intermediate-risk patients. For the exam, remember that TAVR is delivered via a catheter (usually transfemoral) and does not require open heart surgery or cardiopulmonary bypass.

A critical management principle: avoid vasodilators in severe AS. These patients have a fixed obstruction, and reducing afterload can cause precipitous hypotension. However, if a patient with severe AS develops acute heart failure, cautious use of nitroprusside in a monitored setting may be considered.

Regarding prosthetic valve choice: mechanical valves are more durable but require lifelong warfarin anticoagulation (target INR 2.5-3.5 for aortic position). Bioprosthetic (tissue) valves do not require long-term anticoagulation but degenerate over 10-20 years. Young patients (< 50 years) generally receive mechanical valves. Older patients (> 65 years) or those who cannot tolerate anticoagulation receive bioprosthetic valves.

Aortic Regurgitation

For chronic AR, vasodilator therapy (ACE inhibitors, nifedipine, or hydralazine) reduces afterload, promotes forward flow, and decreases the regurgitant fraction. However, per current guidelines, vasodilators are recommended primarily for patients with hypertension or when surgery is not feasible. For asymptomatic patients with normal LV function and no hypertension, watchful waiting with serial echo is appropriate.

In acute AR (endocarditis, aortic dissection), the management is emergent surgery. IV nitroprusside can be used as a bridge. Critically, intra-aortic balloon pump (IABP) is contraindicated in aortic regurgitation because the balloon inflation during diastole would worsen regurgitation. This is a classic board trap.

Mitral Stenosis

Medical therapy focuses on managing the consequences: diuretics reduce pulmonary congestion, and rate control (beta-blockers or non-dihydropyridine calcium channel blockers such as diltiazem and verapamil) is essential in atrial fibrillation to allow adequate diastolic filling time. A fast ventricular rate in MS is dangerous because shorter diastole means less time for blood to flow through the stenotic valve, worsening the transmitral gradient and pulmonary congestion.

Anticoagulation with warfarin is indicated in MS patients who develop atrial fibrillation, prior thromboembolism, or a left atrial thrombus.

For symptomatic moderate-to-severe MS, percutaneous mitral balloon commissurotomy (PMBC) is the intervention of choice if the valve anatomy is favorable. Favorable anatomy means pliable, non-calcified leaflets with no significant MR and no left atrial thrombus (assessed by TEE before the procedure). If anatomy is unfavorable, surgical commissurotomy or valve replacement is performed.

Mitral Regurgitation

In chronic MR, afterload reduction with ACE inhibitors is used when surgery is not feasible or to temporize. Surgical repair (rather than replacement) is the preferred approach for degenerative MR because repair preserves native valve tissue, avoids the need for lifelong anticoagulation, and has better long-term outcomes.

In acute MR (papillary muscle rupture post-MI, chordae rupture), the patient is critically ill. Stabilize with IV vasodilators (nitroprusside) to reduce afterload and decrease the regurgitant fraction, and/or place an IABP (note: IABP is helpful in acute MR but contraindicated in acute AR). Definitive treatment is emergent surgery.

Endocarditis Prophylaxis

For the exam, remember that antibiotic prophylaxis before dental procedures is indicated only for high-risk conditions: prosthetic heart valves, prior endocarditis, certain congenital heart defects, and cardiac transplant patients with valvulopathy. MVP alone, even with regurgitation, does NOT require prophylaxis under current guidelines.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on valvular heart disease questions is by confusing murmur timing and location or by misapplying dynamic auscultation maneuvers. Test-writers know that students memorize murmur characteristics in isolation but fail to apply them when a vignette includes a maneuver. The single highest-yield fact to internalize: almost all murmurs get louder when you increase preload (squatting, leg raise), with the critical exceptions being MVP and HOCM, which behave in the opposite direction. If you understand the physiology behind this (both HOCM and MVP worsen when the LV cavity is smaller), you will never miss these questions.

Another frequent trap involves post-MI complications. A patient who develops a new holosystolic murmur and pulmonary edema 3-5 days after an MI should make you think of papillary muscle rupture causing acute MR. But the test may also offer VSD as an option, which also causes a holosystolic murmur in the post-MI setting. The discriminator is the location and radiation: VSD murmur is at the LLSB with a thrill, while MR murmur is at the apex radiating to the axilla. If the vignette describes a "step-up" in oxygen saturation from the right atrium to the right ventricle on catheterization, that confirms VSD (left-to-right shunt), not MR.

Students also frequently confuse aortic stenosis and HOCM because both present in young patients with syncope, LVH, and a systolic murmur. The vignette will contain a discriminating clue. Look for: a family history of sudden death (HOCM), a murmur that gets louder with Valsalva (HOCM, not AS), asymmetric septal hypertrophy on echo (HOCM), or a bicuspid aortic valve (AS).

The IABP contraindication in aortic regurgitation is tested repeatedly. Students reflexively choose IABP for cardiogenic shock, but in the setting of severe AR, balloon inflation during diastole forces more blood back through the incompetent valve, making regurgitation worse. This same trap does not apply to acute MR, where IABP is beneficial.

Finally, remember the prophylaxis guidelines. Students overtreat by giving antibiotics before dental procedures for MVP. Under current guidelines, MVP (even with regurgitation) is NOT an indication for endocarditis prophylaxis. Only prosthetic valves, prior endocarditis, certain congenital defects, and cardiac transplant valvulopathy qualify.

The core competency being tested across all valve disease questions is the ability to connect pathophysiology to clinical findings, select the correct diagnostic study (which is almost always echocardiography), identify the indication and timing for intervention, and apply hemodynamic principles to murmur differentiation using physical exam maneuvers.