Cardiovascular Drugs (Antihypertensives, Anti-Anginals, Heart Failure, Anti-Arrhythmics) MCQs

Pharmacology · 179 free questions with answers & explanations.

1. Sacubitril/valsartan (LCZ696) is superior to enalapril in HFrEF. The mechanism by which sacubitril contributes to its benefit is:
2. Amiodarone prolongs action potential duration (APD) in cardiac tissue. When used long-term, which toxicity requires periodic monitoring by ophthalmological examination?
3. Hydralazine causes lupus-like syndrome with chronic use. The pharmacogenomic factor that predicts this adverse effect is:
4. Ivabradine reduces heart rate by a novel mechanism and is used in stable angina and HFrEF with sinus tachycardia. Its mechanism of action is:
5. A patient in atrial flutter with rapid ventricular response receives adenosine IV. The expected immediate cardiac effect and its mechanism are:
6. Sacubitril/valsartan (ARNI) is approved for heart failure with reduced ejection fraction (HFrEF). What is the critical washout period required between ACE inhibitor discontinuation and starting sacubitril/valsartan, and why?
7. A patient with SVT on verapamil is inadvertently given IV beta-blocker. Which hemodynamic catastrophe results and what reversal agent is used?
8. Amiodarone-induced thyroid dysfunction occurs in which two distinct patterns, and what is the pharmacological basis for hypothyroidism in susceptible patients?
9. Ivabradine is used in chronic heart failure and stable angina for heart rate reduction. Which unique mechanism differentiates it from beta-blockers?
10. Ranolazine is used for refractory angina. Its novel antianginal mechanism involves:
11. Sacubitril/valsartan (LCZ696) is superior to enalapril in heart failure with reduced ejection fraction. Sacubitril's beneficial hemodynamic effects arise from inhibition of which enzyme?
12. Ivabradine reduces heart rate in stable angina and heart failure WITHOUT affecting myocardial contractility or blood pressure. Its mechanism is:
13. Ranolazine, approved for refractory angina, reduces myocardial ischemia without significantly altering heart rate or blood pressure. Its primary cardioprotective mechanism involves:
14. A patient with hypertrophic obstructive cardiomyopathy (HOCM) presents with drug-refractory left ventricular outflow tract obstruction. Mavacamten has recently been approved for this indication. Its mechanism of action is:
15. Amiodarone prolongs the QT interval and the cardiac action potential. Despite being a class III antiarrhythmic, it has properties of all four Vaughan Williams classes. Its most important limitation in long-term use is:
16. Sacubitril/valsartan (sacubitril being an ARNI — angiotensin receptor-neprilysin inhibitor) reduces mortality in HFrEF. Neprilysin inhibition amplifies the effect of:
17. Ivabradine reduces heart rate in heart failure patients by acting on which specific channel?
18. Amiodarone prolongs the action potential duration primarily by blocking which current, and what is the consequence for refractory period?
19. A hypertensive patient with Type 2 diabetes and microalbuminuria is best treated with which antihypertensive to simultaneously retard the progression of diabetic nephropathy?
20. Nicorandil is used in stable angina pectoris. Its dual mechanism of action involves:
21. Sacubitril/valsartan (LCZ696) reduces mortality in heart failure with reduced ejection fraction. Sacubitril is a prodrug that is converted to the active compound LBQ657 which inhibits which enzyme to augment natriuretic peptide effects?
22. The drug ivabradine lowers heart rate in stable angina and heart failure by selectively blocking which channel without affecting cardiac contractility or conduction?
23. Ranolazine reduces anginal episodes by a mechanism largely independent of heart rate or blood pressure reduction. Its anti-ischemic effect is primarily attributed to:
24. Vernakalant is a new antiarrhythmic drug approved for rapid conversion of recent-onset atrial fibrillation. Its selectivity for atrial tissue over ventricular tissue is explained by:
25. A patient with hypertension and chronic kidney disease stage 3 is found to have hyperkalemia (K+ 5.6 mEq/L) on patiromer therapy. Patiromer lowers serum potassium through which mechanism?
26. Sacubitril/valsartan (LCZ696) is used in HFrEF. Sacubitril inhibits neprilysin, which degrades natriuretic peptides. Why is valsartan (an ARB) combined with sacubitril in this formulation rather than using sacubitril alone?
27. Ivabradine is used in stable angina and HFrEF with heart rate >70 bpm. Its unique mechanism is best described as:
28. A patient with Wolff-Parkinson-White (WPW) syndrome develops atrial fibrillation. Verapamil and digoxin are contraindicated. Which drug is the preferred treatment to terminate the AF and why?
29. Ranolazine is approved for chronic stable angina. Its anti-anginal mechanism is distinct from nitrates, beta-blockers, and calcium channel blockers. It acts by inhibiting:
30. The pharmacogenomic test most relevant to deciding clopidogrel dose adequacy in a patient with coronary artery disease is genotyping for:
31. Sacubitril/valsartan (LCZ696) reduces mortality in HFrEF beyond valsartan alone. The additional benefit of sacubitril is mediated by:
32. Ivabradine reduces heart rate by a unique mechanism relevant to sinoatrial node automaticity. It blocks the:
33. A patient with paroxysmal atrial fibrillation is given vernakalant IV. Its clinical advantage over flecainide for acute cardioversion of AF relates to its atrial selectivity, which is due to preferential blockade of:
34. Ranolazine reduces anginal episodes by a mechanism independent of heart rate or blood pressure lowering. It acts by inhibiting:
35. A 68-year-old with HFrEF and CKD stage 3 is started on finerenone. Finerenone differs from spironolactone's aldosterone antagonism in HF management primarily because finerenone:
36. Sacubitril-valsartan (LCZ696) differs from plain valsartan in its mechanism. Which enzyme does sacubitril's active metabolite LBQ657 inhibit, and what is the principal benefit?
37. Ivabradine reduces heart rate without negative inotropy. Which mechanism underpins this property, and in which specific patient population is it most indicated?
38. A patient develops proarrhythmia after initiation of flecainide for paroxysmal atrial fibrillation. Which specific arrhythmia mechanism is flecainide most likely to have unmasked or facilitated?
39. Empagliflozin (SGLT2 inhibitor) has demonstrated mortality benefit in heart failure with reduced ejection fraction independent of its glucose-lowering effect. Which is the most mechanistically convincing explanation?
40. Sacubitril/valsartan (LCZ696) is a first-in-class ARNI (angiotensin receptor-neprilysin inhibitor). Neprilysin inhibition reduces the degradation of natriuretic peptides. What is the clinical risk created by combining neprilysin inhibition with an ACE inhibitor (rather than an ARB)?
41. Ivabradine is used in heart failure patients in sinus rhythm with HR ≥70 bpm. Its mechanism — inhibition of the 'funny current' (If) — specifically targets which ion channel, and what property makes it rate-dependent in effect?
42. Amiodarone prolongs the QT interval through potassium channel blockade (class III effect). Despite QT prolongation, amiodarone has a LOWER risk of torsades de pointes compared to sotalol. The most likely explanation is:
43. Riociguat is approved for pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). Its mechanism — direct stimulation of soluble guanylate cyclase (sGC) — differs from sildenafil in what way?
44. A 55-year-old man with hypertension and type 2 diabetes is on an ACE inhibitor. Eplerenone is added for cardiovascular protection. Compared to spironolactone, eplerenone is preferred primarily because:
45. Sacubitril/valsartan (LCZ696) is superior to enalapril in HFrEF because the neprilysin inhibition component:
46. Ivabradine reduces heart rate in heart failure without affecting contractility because it selectively:
47. The SGLT2 inhibitor empagliflozin reduces hospitalization for heart failure in patients with HFrEF via a mechanism that goes beyond glycemic control. The primary proposed hemodynamic mechanism involves:
48. A patient with ventricular tachycardia is given amiodarone. The primary electrophysiological mechanism responsible for its broad-spectrum antiarrhythmic efficacy is:
49. Sacubitril/valsartan (LCZ696) is superior to enalapril in HFrEF (PARADIGM-HF). The pharmacodynamic rationale for adding neprilysin inhibition to RAAS blockade is:
50. A 58-year-old with heart failure with preserved ejection fraction (HFpEF) and type 2 diabetes started on empagliflozin shows symptomatic improvement. The mechanism responsible for HFpEF benefit beyond glycemic control is BEST explained by:
51. Amiodarone-induced thyrotoxicosis type 2 (AIT-2) is managed differently from type 1 (AIT-1). The distinction and treatment of AIT-2 is:
52. Ivabradine reduces heart rate in stable angina and chronic HFrEF. Its mechanism of action, different from β-blockers, is:
53. A patient on warfarin for AF is started on rifampicin for tuberculosis. The INR drops from 2.5 to 1.2 after two weeks. The molecular mechanism of this interaction is:
54. Sacubitril/valsartan (Entresto) is used in heart failure with reduced ejection fraction. Sacubitril's mechanism involves inhibition of which enzyme, and what is the resulting pharmacological consequence?
55. Ivabradine is used for heart failure and stable angina in patients with contraindications to beta blockers. Its mechanism of action is best described as:
56. A patient with hypertension and CKD with proteinuria is started on an ACE inhibitor. The reno-protective mechanism of ACEi in diabetic nephropathy, beyond blood pressure lowering, primarily involves:
57. A patient with recurrent ventricular tachycardia is treated with amiodarone. Amiodarone's predominant antiarrhythmic mechanism involves which of the following, and which class of action does this classify it under?
58. Sacubitril/valsartan (LCZ696) reduces mortality in heart failure with reduced ejection fraction. What is the mechanism of sacubitril's active metabolite?
59. Ivabradine reduces heart rate without affecting myocardial contractility or blood pressure. The molecular target responsible for this selective chronotropic effect is:
60. A 58-year-old man on amiodarone for atrial fibrillation develops thyrotoxicosis. Which mechanism of amiodarone-induced thyroid dysfunction is characterized by absent vascularity on color Doppler ultrasound?
61. Ranolazine exerts anti-anginal effects without significant hemodynamic changes. Its primary mechanism targets which ion channel abnormality in ischemic myocardium?
62. Ivabradine reduces heart rate in heart failure patients with sinus rhythm by selectively blocking:
63. A patient with chronic heart failure and reduced ejection fraction (HFrEF) is started on sacubitril-valsartan. The mechanism by which sacubitril enhances its cardiovascular benefit is:
64. In Wolf-Parkinson-White syndrome complicated by atrial fibrillation, the drug that is absolutely contraindicated due to risk of ventricular fibrillation is:
65. Hydralazine lowers blood pressure through which primary sub-mechanism at the vascular smooth muscle level?
66. A patient with stable angina is started on ranolazine. Its anti-anginal mechanism involves:
67. Digoxin toxicity manifests with bradyarrhythmias and ventricular ectopics. At the cellular level, digoxin toxicity arises from:
68. Sacubitril/valsartan (LCZ696) is approved for heart failure with reduced ejection fraction (HFrEF). The pharmacological advantage of neprilysin inhibition (sacubitril) in combination with ARB (valsartan) over ACE inhibitor alone is:
69. A patient with atrial fibrillation on amiodarone is started on warfarin. The expected interaction and the correct dose adjustment is:
70. The unique mechanism of ivabradine's heart rate reduction — distinct from beta-blockers — is through:
71. A patient with hypertrophic obstructive cardiomyopathy (HOCM) who is symptomatic despite maximally tolerated doses of beta-blocker is now started on mavacamten. Its mechanism of action is:
72. Ivabradine reduces heart rate in stable angina by:
73. A 55-year-old man with heart failure (EF 30%) is started on sacubitril/valsartan. The sacubitril component acts as:
74. According to the Vaughan Williams classification, amiodarone is primarily classified as a Class III antiarrhythmic. However, it also has additional actions including:
75. Which anti-hypertensive drug class is specifically contraindicated in bilateral renal artery stenosis because it removes the angiotensin II-dependent efferent arteriolar tone that maintains GFR?
76. A patient has atrial fibrillation with rapid ventricular rate and is haemodynamically stable. Adenosine is administered. This drug terminates paroxysmal supraventricular tachycardia primarily by:
77. A 72-year-old patient is in cardiogenic shock post-MI with refractory hypotension. Which vasopressor/inotrope combination best balances increasing MAP while avoiding excessive tachycardia and increased myocardial oxygen demand?
78. Hydralazine combined with isosorbide dinitrate is specifically indicated for heart failure in which patient population, and why is ACE inhibitor/ARB preferred over this combination in most patients?
79. Ivabradine reduces heart rate by a mechanism different from beta-blockers. It acts by:
80. Sacubitril/valsartan (LCZ696) reduces mortality in HFrEF. The sacubitril component acts as a prodrug; its active metabolite LBQ657 inhibits which enzyme?
81. Amiodarone's classification as a class III antiarrhythmic is based on potassium channel blockade, but it also possesses actions of which other Vaughan-Williams classes?
82. A 55-year-old with chronic stable angina is on a calcium channel blocker. The drug causes significant reflex tachycardia due to its strong peripheral vasodilation. Which drug is most likely?
83. Ivabradine reduces heart rate by selectively blocking the If (funny current) channel. In which specific cell type and at what phase of the action potential does this occur?
84. Sacubitril is a prodrug that is converted to the active form LBQ657. What is the enzymatic target of LBQ657 and what is the pharmacodynamic consequence?
85. Adenosine is used for acute conversion of paroxysmal SVT. Its ultra-short duration of action (~10 seconds) is due to:
86. In a patient with chronic heart failure with reduced EF, which SGLT2 inhibitor has demonstrated reduction in both cardiovascular death/hospitalisation for HF and progression of CKD, regardless of diabetes status?
87. Amiodarone prolongs the QT interval and can cause torsades de pointes, yet paradoxically it is LESS arrhythmogenic than other class III drugs. This is because amiodarone also blocks:
88. Ivabradine reduces heart rate in stable angina by blocking which ion channel?
89. A patient in acute decompensated heart failure is given sacubitril/valsartan. Sacubitril inhibits neprilysin; which endogenous peptides accumulate as a result?
90. Amiodarone belongs to Class III antiarrhythmics and prolongs the cardiac action potential. However, at therapeutic concentrations it also blocks which other ion channels, contributing to its broad antiarrhythmic spectrum?
91. A 55-year-old woman with hypertension is prescribed hydralazine. The primary mechanism by which hydralazine lowers blood pressure is:
92. Digoxin toxicity in a patient with atrial fibrillation is worsened by hypokalaemia. The mechanism involves:
93. Ivabradine is used for rate control in chronic stable angina and heart failure. Its mechanism of action is:
94. Sacubitril-valsartan (LCZ696) is used in HFrEF. Sacubitril's active metabolite LBQ657 improves haemodynamics by:
95. A patient with Wolff-Parkinson-White syndrome develops atrial fibrillation. Which of the following drugs is CONTRAINDICATED because it can paradoxically accelerate ventricular rate?
96. The class III antiarrhythmic action of sotalol differs from other class III agents like amiodarone because sotalol:
97. Which antihypertensive drug is the ONLY one known to cause drug-induced lupus erythematosus through a mechanism involving inhibition of complement and generation of reactive oxygen species from neutrophil myeloperoxidase?
98. Ivabradine is used in heart failure with preserved ejection fraction and as add-on to beta-blockers in stable angina. Its mechanism of heart rate reduction involves:
99. A patient with heart failure with reduced ejection fraction (HFrEF) is started on sacubitril-valsartan (Entresto). The addition of sacubitril provides benefit primarily by:
100. A patient with WPW syndrome and atrial fibrillation is brought to the ED with rapid ventricular rate via the accessory pathway. Which drug is CONTRAINDICATED in this situation?
101. Ranolazine is an antianginal drug approved as add-on therapy when beta-blockers and nitrates are insufficient. Its mechanism is:
102. Amiodarone has a uniquely long half-life of approximately 40–55 days. The primary pharmacokinetic reason for this is:
103. Digoxin toxicity is worsened by hypokalemia. The mechanism linking hypokalemia to increased digoxin toxicity is:
104. Eplerenone is preferred over spironolactone in post-MI patients with left ventricular dysfunction (EPHESUS trial) for long-term treatment because:
105. A 68-year-old man with HFrEF is on lisinopril, carvedilol, and furosemide. His physician adds sacubitril/valsartan (Entresto) but first discontinues lisinopril. The mandatory 36-hour washout period before starting sacubitril/valsartan is required to prevent:
106. A patient with Wolff-Parkinson-White (WPW) syndrome presents with a wide-complex tachycardia. The cardiology team avoids IV adenosine, IV verapamil, and IV diltiazem. The reason for avoiding these agents in WPW with pre-excitation is:
107. Ivabradine is added to therapy in a 70-year-old patient with stable heart failure (LVEF 30%) who is already on maximum-dose carvedilol. The unique electrophysiological mechanism of ivabradine that distinguishes it from beta-blockers is:
108. A 60-year-old male with persistent AF is started on dronedarone. His physician checks renal and hepatic function. Dronedarone is contraindicated in patients with permanent AF or NYHA class III-IV heart failure because clinical trials demonstrated:
109. A 55-year-old man with hypertension is on amlodipine 10 mg/day. His blood pressure remains uncontrolled. His physician adds telmisartan. This combination is preferred over the ACE inhibitor-CCB combination in elderly patients primarily because telmisartan:
110. Ivabradine reduces heart rate by blocking the funny current (If). This current flows through HCN (hyperpolarization-activated cyclic nucleotide-gated) channels. The unique clinical advantage of ivabradine over beta-blockers for rate control is:
111. Sacubitril/valsartan (LCZ696) is a combination drug approved for HFrEF. The sacubitril component acts as a prodrug and exerts its benefit by inhibiting which enzyme?
112. Ranolazine is used as an add-on anti-anginal agent. Its mechanism of action that reduces myocardial oxygen demand without affecting heart rate or blood pressure is:
113. A patient develops torsades de pointes arrhythmia after starting a class IA antiarrhythmic. This proarrhythmic complication is due to excessive blockade of which ion channel?
114. Which antihypertensive drug reduces both preload and afterload, is the drug of choice in hypertensive emergency with acute LV failure, and acts primarily by releasing nitric oxide?
115. Vernakalant is an antiarrhythmic approved in Europe specifically for rapid conversion of recent-onset atrial fibrillation. Its unique mechanism compared to other antiarrhythmics is:
116. Milrinone is a positive inotrope used for acute decompensated heart failure. Its mechanism of action is:
117. Ivabradine is used in stable angina and heart failure. Its mechanism differs from beta-blockers in that ivabradine:
118. A patient with atrial fibrillation has a rapid ventricular response despite adequate beta-blockade. Digoxin is added. The mechanism by which digoxin slows ventricular rate in AF is:
119. Sacubitril-valsartan is used in HFrEF. The component sacubitril acts by:
120. Amiodarone is classified as a Vaughan-Williams class III antiarrhythmic but also exhibits properties of classes I, II, and IV. Its predominant electrophysiological effect is:
121. A patient with Prinzmetal (variant) angina is best managed with which of the following drug classes?
122. Ivabradine reduces heart rate in heart failure by blocking the If (funny) current. Which ion channels constitute the If current and where are they located?
123. A 55-year-old with hypertension is started on sacubitril/valsartan (Entresto). Sacubitril works by inhibiting neprilysin. Which of the following peptides most accurately summarizes the substrates whose degradation is inhibited by neprilysin?
124. Amiodarone is a Class III antiarrhythmic with a complex pharmacokinetic profile. Which of the following statements about amiodarone pharmacokinetics is CORRECT?
125. A patient with stable angina is given ranolazine as add-on therapy. The anti-ischemic mechanism of ranolazine is best described as:
126. Among the following antihypertensive agents, which one is a direct renin inhibitor that acts at the first and rate-limiting step of the RAAS?
127. A patient with heart failure with reduced ejection fraction (HFrEF) is started on sacubitril-valsartan (Entresto). What is the mechanism of the sacubitril component?
128. A patient with hypertension and chronic kidney disease (CKD stage 3) is on maximum tolerated dose of ACE inhibitor. An aldosterone breakthrough phenomenon occurs. Which drug, when added, addresses this specifically by antagonizing the mineralocorticoid receptor?
129. Amiodarone is used for both atrial fibrillation and ventricular arrhythmias because it acts on multiple ion channels. Amiodarone is classified as which Vaughan-Williams class, and why is this classification considered an oversimplification?
130. A patient with stable angina continues to have anginal episodes despite maximum beta-blocker therapy. Ivabradine is added. The molecular target of ivabradine is:
131. Ivabradine reduces heart rate in stable angina by a mechanism distinct from beta-blockers. It specifically inhibits which cardiac channel?
132. A 65-year-old patient with heart failure with reduced ejection fraction (HFrEF) is started on sacubitril/valsartan. The sacubitril component acts as a prodrug converted to sacubitrilat, which inhibits which enzyme to produce its haemodynamic benefits?
133. Amiodarone is a Class III antiarrhythmic but also has Class I, II and IV properties. Its major pharmacokinetic characteristic that explains why a loading dose is mandatory and toxicities persist long after drug withdrawal is:
134. Which antihypertensive drug class is the preferred agent in hypertensive patients with unilateral renal artery stenosis and is potentially harmful due to a specific haemodynamic mechanism?
135. Hydralazine produces direct arteriolar vasodilation but consistently causes reflex tachycardia and salt retention. To counter these, it is typically combined with which pair of drugs for heart failure management?
136. Sacubitril in the combination sacubitril/valsartan (Entresto) acts as a prodrug for LBQ657. The mechanism of LBQ657 that benefits heart failure is:
137. Ivabradine reduces heart rate without affecting myocardial contractility or blood pressure. Its mechanism is:
138. Amiodarone belongs to Vaughan-Williams class III but also has properties of classes I, II, and IV. Its most dangerous long-term adverse effect requiring regular monitoring is:
139. Hydralazine is an arterial vasodilator used in hypertensive emergencies in pregnancy. Its mechanism of vasodilation is:
140. Digoxin's positive inotropic effect in heart failure is mediated through:
141. Sacubitril/valsartan (LCZ696) improves outcomes in HFrEF. Sacubitril inhibits neprilysin. Which peptides accumulate as a direct result of neprilysin inhibition?
142. Ivabradine reduces heart rate without affecting contractility or blood pressure. Its target is:
143. Ranolazine is used as adjunctive anti-anginal therapy. Its anti-ischemic effect is mediated by inhibition of:
144. A 60-year-old patient with recurrent paroxysmal AF and structural heart disease (EF 35%) requires rhythm control. Which antiarrhythmic is MOST appropriate?
145. Hydralazine causes reflex tachycardia when used alone for hypertension. This reflex is mediated primarily by:
146. Ivabradine lowers heart rate without affecting myocardial contractility or blood pressure because it selectively inhibits:
147. Ranolazine reduces angina frequency by a mechanism that differs from nitrates and beta-blockers. Its primary mechanism is:
148. Sacubitril, used in heart failure with reduced EF, inhibits neprilysin. The combined effect of sacubitril/valsartan results in all of the following EXCEPT:
149. Amiodarone prolongs the QT interval primarily by blocking which ion channel?
150. Sodium nitroprusside (SNP) toxicity manifests as lactic acidosis because:
151. Ivabradine reduces heart rate in heart failure by selectively blocking the If (funny) current. Compared to beta-blockers, ivabradine's mechanism of action is clinically distinct because it:
152. A patient with atrial fibrillation and Wolff-Parkinson-White syndrome presents to the emergency department. Administration of which drug is most dangerous in this setting?
153. Sacubitril is combined with valsartan (LCZ696/Entresto) in heart failure. The mechanism by which sacubitril provides benefit beyond ACE inhibitor therapy is:
154. Hydralazine combined with isosorbide dinitrate is an alternative to ACE inhibitors in heart failure patients with renal failure. Hydralazine's mechanism of reducing cardiac afterload is:
155. A 65-year-old patient with heart failure with reduced ejection fraction (HFrEF, EF 30%) is already on maximally tolerated doses of ACE inhibitor, beta-blocker, and mineralocorticoid antagonist. The cardiologist now adds sacubitril-valsartan. What is the molecular rationale for replacing the ACE inhibitor with this combination?
156. A 70-year-old woman with chronic atrial fibrillation is anticoagulated with rivaroxaban. She is started on amiodarone for rate control. Two weeks later, her laboratory results show unexpectedly elevated rivaroxaban plasma levels with increased bleeding risk. What is the mechanism of this interaction?
157. Ranolazine is approved for chronic stable angina refractory to other agents. Unlike conventional anti-anginals, it does not reduce heart rate or blood pressure at therapeutic doses. What is its unique anti-ischemic mechanism?
158. A patient is in the CCU with acute MI and develops ventricular fibrillation. After defibrillation, persistent ventricular ectopics continue. IV amiodarone is administered. Amiodarone primarily belongs to Vaughan Williams class III, but it also exhibits properties of classes I, II, and IV. Which unique pharmacological property makes IV amiodarone the preferred choice over lidocaine in shock-refractory VF/VT?
159. SGLT2 inhibitors (empagliflozin, dapagliflozin) have demonstrated significant cardiovascular mortality reduction in heart failure patients even without diabetes. What is the proposed primary mechanism for their cardiac benefit?
160. Sacubitril is a neprilysin inhibitor. When combined with valsartan in the ARNI sacubitril/valsartan (LCZ696), a crucial risk that was the main reason it cannot be combined with ACE inhibitors is:
161. Ivabradine reduces heart rate by blocking funny current (If) channels in the sino-atrial node. Unlike β-blockers, it is preferred in which clinical scenario?
162. Amiodarone prolongs the action potential duration (class III effect) by blocking rapidly activating delayed rectifier potassium channels (IKr). Its loading dose requirement is explained by which pharmacokinetic property?
163. Empagliflozin (SGLT2 inhibitor) reduces hospitalisation for heart failure with reduced EF (HFrEF) independent of its glucose-lowering effect. The proposed cardioprotective mechanism involves:
164. Amiodarone inhibits potassium channels as its primary antiarrhythmic mechanism. Based on the Vaughan Williams classification, it is a Class III drug but also exhibits properties of which other classes?
165. Ivabradine reduces heart rate in chronic heart failure. Its mechanism is unique because:
166. Sacubitril (combined with valsartan as sacubitril/valsartan) improves outcomes in heart failure with reduced ejection fraction by inhibiting:
167. Nicorandil is used in refractory angina. Its dual mechanism of action includes:
168. A patient taking atorvastatin develops severe myopathy after adding gemfibrozil for hypertriglyceridemia. The pharmacokinetic basis of this interaction is:
169. Ivabradine reduces heart rate in stable angina without affecting myocardial contractility or blood pressure. Its mechanism is:
170. Sacubitril is combined with valsartan in heart failure with reduced ejection fraction. The target enzyme inhibited by sacubitril's active metabolite (LBQ657) is:
171. Class III antiarrhythmic drugs like amiodarone prolong the QT interval by blocking:
172. A patient with pheochromocytoma crisis is being prepared for surgery. The sequence of drug administration should be:
173. Ranolazine reduces anginal episodes without affecting heart rate or blood pressure. Its primary anti-ischaemic mechanism is:
174. Digoxin toxicity is markedly worsened by hypokalemia. The mechanism is:
175. A 68-year-old man with diastolic heart failure and atrial fibrillation is treated with a rate-control drug. Which drug is CONTRAINDICATED in hypertrophic obstructive cardiomyopathy (HOCM)?
176. A patient with paroxysmal supraventricular tachycardia (PSVT) is successfully cardioverted with adenosine IV. The haemodynamic mechanism by which adenosine terminates SVT is:
177. A patient on digoxin develops toxicity. The toxic manifestations include ventricular extrasystoles (DADs — delayed afterdepolarisations) arising from which mechanism?
178. Digoxin toxicity is worsened by hypokalaemia because:
179. A patient is started on hydralazine and isosorbide dinitrate combination for heart failure with reduced ejection fraction after failing ACE inhibitor and ARB due to intolerance. The mechanism of benefit is: