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1
Question:

A 22-year-old man comes to the office due to a 6-month history of difficulty breathing and chest discomfort on exertion.  He also reports intermittent palpitations.  The patient's only other medical condition is major depression.  Temperature is 37 C (98.6 F), blood pressure is 120/80 mm Hg, pulse is 82/min, and respirations are 15/min.  Pulse oximetry on room air shows an oxygen saturation of 98%.  BMI is 24 kg/m2.  The lungs are clear on auscultation.  Cardiac examination reveals a prominent left ventricular impulse on palpation, an S4, and a faint systolic murmur at the left sternal border that accentuates during the strain phase of the Valsalva maneuver.  Verapamil therapy would most likely improve this patient's dyspnea through which of the following mechanisms?

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Hypertrophic cardiomyopathy

Inheritance

  • Autosomal dominant with incomplete penetrance
  • Mutations affecting proteins of the cardiac sarcomere
  • Most common: myosin-binding protein C & β-myosin heavy chain

Phenotypic
manifestations

  • Myocardial disarray & coronary microvascular dysfunction
  • Asymmetric septal hypertrophy with dynamic LVOT obstruction
  • LV stiffening with diastolic dysfunction
  • Increased risk of ventricular arrhythmias & SCD

Clinical
presentation

  • Often asymptomatic
  • Exertional dyspnea, angina, palpitations, light-headedness, syncope
  • Systolic murmur that increases in intensity with ↓ LV blood volume
  • Audible S4

LV = left ventricular; LVOT = left ventricular outflow tract; SCD = sudden cardiac death.

A systolic murmur at the left sternal border that increases in intensity with maneuvers that decrease left ventricular (LV) blood volume is characteristic of hypertrophic cardiomyopathy (HCM).  The murmur is caused by dynamic LV outflow tract obstruction that worsens with relatively low LV blood volume and improves with relatively high LV blood volume.  Other common physical examination findings include an S4 (caused by LV wall-thickening with diastolic dysfunction) and prominent LV impulse.  Patients may be asymptomatic or have palpitations and/or exertional symptoms, including dyspnea, chest pain, lightheadedness, and syncope.

Pharmacologic management of HCM focuses on maintaining relatively high LV blood volume throughout the cardiac cycle, which minimizes LV outflow tract obstruction and associated symptoms.  This is best accomplished via 2 mechanisms:

  • Negative chronotropy (ie, reduced heart rate), which lengthens diastolic filling time to increase LV end-diastolic volume (ie, preload)
  • Negative inotropy (ie, reduced LV contractility), which decreases the amount of blood ejected during ventricular systole (ie, increased end-systolic volume)

Beta blockers and nondihydropyridine calcium channel blockers (eg, verapamil) are used in HCM to provide negative chronotropy and inotropy and reduce symptoms related to outflow tract obstruction.

(Choice A)  Decreased LV afterload is primarily caused by arterial dilators (eg, ACE inhibitors, dihydropyridine calcium channel blockers such as amlodipine) and is detrimental in HCM as it reduces LV blood volume to worsen LVOT obstruction.  Verapamil has no significant vasodilatory effect on systemic vessels.

(Choices B and C)  The negative chronotropy of verapamil decreases atrioventricular conduction velocity to lengthen diastolic filling time and increase LV end-diastolic cavity size.  An increase in atrioventricular conduction velocity (eg, as occurs with exercise) tends to decrease LV end-diastolic cavity size and worsen LV outflow tract obstruction.

(Choice E)  The negative inotropy of verapamil decreases myocardial contraction velocity.  Increased contraction velocity can worsen LV outflow tract obstruction by reducing end-systolic volume.

Educational objective:
Hypertrophic cardiomyopathy commonly involves dynamic left ventricular (LV) outflow tract obstruction that worsens with decreased LV blood volume and improves with increased LV blood volume.  Nondihydropyridine calcium channel blockers (eg, verapamil) decrease heart rate (ie, negative chronotropy) and LV contractility (ie, negative inotropy) to increase LV blood volume, reduce LV outflow tract obstruction, and improve symptoms.