Cardiovascular Disease Flashcards

A 58-year-old man with hypertension and type 2 diabetes presents with exertional dyspnea. Echocardiography shows an EF of 58%, grade II diastolic dysfunction, E/e' ratio of 16, and left atrial volume index of 42 mL/m². He is started on an SGLT2 inhibitor. Which mechanism BEST explains its cardiovascular benefit in heart failure with preserved ejection fraction (HFpEF)?

Answer: Reduction of preload via osmotic diuresis and natriuresis, reducing myocardial wall stress

SGLT2 inhibitors reduce hospitalizations and cardiovascular death in HFpEF (EMPEROR-Preserved trial with empagliflozin; DELIVER trial with dapagliflozin). The primary hemodynamic mechanism is osmotic diuresis and natriuresis, which reduces intravascular volume, lowers ventricular filling pressures (preload), and decreases myocardial wall stress — a critical pathophysiologic driver in HFpEF. They do not directly inhibit RAAS, upregulate beta receptors, or act as NCX inhibitors.

A 44-year-old woman presents with recurrent syncope and palpitations. Holter monitoring captures a polymorphic ventricular tachycardia triggered exclusively by catecholamine surges (emotion, exercise). She has a structurally normal heart, normal QTc (440 ms), and a family history of sudden death in young relatives. Genetic testing is most likely to reveal a mutation in which gene?

Answer: RYR2

This clinical picture — catecholamine-triggered bidirectional or polymorphic VT, structurally normal heart, normal QTc, and family history of sudden death — is classic for catecholaminergic polymorphic ventricular tachycardia (CPVT). The most common causative mutation is in RYR2, encoding the cardiac ryanodine receptor (type 2), which regulates sarcoplasmic reticulum calcium release. Abnormal 'leaky' RYR2 during adrenergic stimulation causes spontaneous calcium sparks and delayed afterdepolarizations triggering VT. KCNQ1 and KCNH2 mutations cause Long QT syndrome types 1 and 2; SCN5A mutations cause LQTS type 3 or Brugada syndrome.

A 67-year-old man with a prior STEMI (2 years ago) is found to have an EF of 30%. He is on maximally tolerated guideline-directed medical therapy including sacubitril-valsartan, carvedilol, eplerenone, and dapagliflozin. His current NYHA class is II, HR is 72 bpm in sinus rhythm, BP is 108/66 mmHg. He has a LBBB with QRS duration of 158 ms. Which intervention has the strongest mortality benefit at this stage?

Answer: Cardiac resynchronization therapy with defibrillator (CRT-D) implantation

This patient meets optimal CRT-D criteria: EF ≤35%, LBBB morphology with QRS ≥150 ms, NYHA class II on GDMT, and sinus rhythm. CRT-D reduces all-cause mortality by ~36% in this population (MADIT-CRT, REVERSE trials) and provides superior benefit over ICD alone due to the reverse remodeling effect of resynchronization, which can meaningfully improve EF. Ivabradine is indicated when HR ≥70 bpm on maximally tolerated beta-blocker in sinus rhythm — his HR of 72 is borderline and the QRS abnormality is the dominant remediable finding. ICD alone would not address dyssynchrony. Transplant is premature for NYHA class II.

A 52-year-old woman presents with acute-onset chest pain that began while arguing with a family member. ECG shows diffuse ST elevation with deep T-wave inversions in precordial leads. Troponin-I peaks at 1.8 ng/mL. Emergent coronary angiography reveals no obstructive coronary artery disease. Left ventriculography demonstrates apical ballooning with basal hyperkinesis. Cardiac MRI shows myocardial edema but no late gadolinium enhancement. What is the most feared in-hospital complication of her condition?

Answer: Dynamic left ventricular outflow tract obstruction with cardiogenic shock

This is Takotsubo (stress) cardiomyopathy, characterized by apical ballooning, emotional/physical trigger, no obstructive CAD, and absent late gadolinium enhancement. The most feared acute hemodynamic complication is dynamic LVOT obstruction, occurring in up to 10–20% of cases. Basal hypercontractility combined with reduced cavity size from catecholamine surge creates a Venturi effect, causing systolic anterior motion (SAM) of the mitral valve and obstruction. This can precipitate cardiogenic shock — paradoxically worsened by inotropes or volume depletion. Free-wall rupture and complete heart block are far more characteristic of STEMI. Apical thrombus can form but massive PE from it acutely is rare.

A 71-year-old man with severe aortic stenosis (AVA 0.7 cm², mean gradient 52 mmHg) and EF of 25% is evaluated for intervention. Despite optimizing heart failure therapy, his EF remains 25%. Dobutamine stress echocardiography shows a rise in mean gradient to 68 mmHg with valve area increasing to only 0.82 cm², and contractile reserve (EF increases to 35%) is demonstrated. What does this response MOST accurately indicate?

Answer: True severe AS with contractile reserve: the patient is higher risk but likely to benefit from AVR/TAVR

In low-flow, low-gradient severe AS (EF <50%, mean gradient <40 mmHg), dobutamine stress echo distinguishes true severe AS from pseudo-severe AS and identifies contractile reserve. Here, the gradient rises (≥40 mmHg under stress) and valve area remains <1.0 cm² (0.82 cm²) — confirming true severe AS. Contractile reserve (EF improvement ≥10 percentage points) is demonstrated. This combination predicts a favorable surgical/TAVR outcome with ~70% chance of EF improvement post-intervention. In pseudo-severe AS, the valve area would normalize to ≥1.0 cm² at higher flows. Lack of contractile reserve (no EF rise) confers high operative risk but intervention may still be considered.

A 38-year-old woman with systemic lupus erythematosus (SLE) presents with progressive exertional dyspnea. Right heart catheterization shows: mPAP 38 mmHg, PCWP 10 mmHg, PVR 5.2 Wood units, cardiac output 4.1 L/min. ANA is positive; anti-dsDNA and anti-cardiolipin antibodies are elevated. She has no interstitial lung disease on HRCT. She is started on disease-modifying therapy for SLE. Which additional management is MOST appropriate for her pulmonary hypertension?

Answer: Combination upfront therapy with an endothelin receptor antagonist plus a PDE-5 inhibitor

This patient has WHO Group 1 pulmonary arterial hypertension associated with connective tissue disease (CTD-PAH, specifically SLE). Her hemodynamics confirm pre-capillary PH (PCWP ≤15 mmHg, elevated PVR >3 WU). Upfront combination therapy (ERA + PDE-5i, e.g., ambrisentan + tadalafil, proven in AMBITION trial) is the standard of care for intermediate-to-high risk PAH, which this patient meets given her hemodynamic profile. Anticoagulation in PAH-CTD (unlike idiopathic PAH) has not shown benefit and may increase bleeding risk, especially with anti-cardiolipin antibodies unless antiphospholipid syndrome with thrombosis exists. CCB therapy requires acute vasoreactivity testing (rare in CTD-PAH, <1% respond). Corticosteroids treat the SLE but are not vasodilators.