Reversal of inappropriate peripheral vascular responses in hypertrophic cardiomyopathy

Rajesh Thaman1, Perry M Elliott, Jaymin S Shah

  • 1Department of Cardiological Sciences, St. George's Hospital Medical School, London, United Kingdom. rajesh.thaman@uclh.nhs.uk

Insights

Abnormal forearm vasodilation occurs in 40% of hypertrophic cardiomyopathy patients with exercise blood pressure issues. Medications like propranolol, clonidine, and paroxetine reversed these responses.

Area of Science:

  • Cardiology
  • Autonomic Nervous System Research
  • Pharmacology

Background:

  • Some hypertrophic cardiomyopathy (HCM) patients exhibit abnormal blood pressure response (ABPR) to exercise, potentially due to paradoxical peripheral vasodilation.
  • Central volume unloading via lower body negative pressure (LBNP) reveals similar paradoxical forearm vasodilation in a subset of HCM patients.
  • These abnormal reflexes may stem from left ventricular mechanoreceptor activation, a mechanism potentially implicated in vasovagal syncope.

Purpose of the Study:

  • To determine the frequency of abnormal forearm vasodilator responses during LBNP in HCM patients with ABPR during exercise.
  • To evaluate the efficacy of propranolol, clonidine, and paroxetine in treating these abnormal vascular responses and exercise blood pressure issues.

Main Methods:

  • Assessed blood pressure changes during exercise.
  • Utilized plethysmography to measure forearm vascular responses and baroreceptor sensitivity during LBNP.
  • Conducted a double-blind crossover study involving 21 non-obstructive HCM patients with ABPR.

Main Results:

  • 43% of patients (group A) displayed paradoxical vasodilator responses during LBNP, while 57% (group B) showed normal vasoconstrictor responses.
  • Paroxetine improved systolic blood pressure (SBP) during exercise in group A and reversed paradoxical LBNP responses in 78% of these patients.
  • Propranolol and clonidine demonstrated efficacy in reversing paradoxical vascular responses in some patients from group A.

Conclusions:

  • Paradoxical forearm vasodilatation during LBNP is observed in approximately 40% of HCM patients with exercise-induced ABPR.
  • Propranolol, clonidine, and paroxetine effectively reversed these abnormal vasodilatory responses.
  • Paroxetine demonstrated an additional benefit by improving the SBP response to exercise in affected patients.
Abstract

Related Concept Videos

Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...