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[Nifedipine in the treatment of hypertrophic non-obstructive cardiomyopathy]
Insights
Nifedipine improves diastolic filling in patients with hypertrophic cardiomyopathy. This medication enhances left ventricular relaxation and filling dynamics, offering a potential treatment for the nonobstructive form of the disease.
Area of Science:
- Cardiology
- Pharmacology
Context:
- Hypertrophic cardiomyopathy (HCM) involves a stiff, hypertrophied left ventricle, impacting cardiac function.
- The noncompliant left ventricle is central to HCM pathophysiology, with or without outflow tract obstruction.
Purpose:
- To evaluate the effects of nifedipine on left ventricular (LV) diastolic filling and relaxation in patients with nonobstructive HCM.
- To assess echocardiographic parameters of LV diastolic function after oral nifedipine administration.
Summary:
- In 11 patients with nonobstructive HCM, nifedipine (10 mg orally) was administered.
- Echocardiograms measured LV diastolic filling parameters, including isovolumic relaxation time (IVRT), maximal fiber lengthening velocity (-VCF), and percent diameter increase during rapid filling (%DRF).
- Nifedipine reduced blood pressure, decreased IVRT, and increased -VCF and %DRF, indicating improved LV relaxation and diastolic filling.
Impact:
- Nifedipine demonstrated a significant improvement in diastolic filling dynamics in patients with nonobstructive hypertrophic cardiomyopathy.
- These findings suggest nifedipine's potential utility in managing the nonobstructive variant of HCM.
Abstract:
The left ventricle of patients with hypertrophic cardiomyopathy is typically asymmetrically hypertrophied and noncompliant. The stiff, hypertrophied left ventricle plays a key role in the pathophysiology of hypertrophic cardiomyopathy with and without an outflow tract gradient. In 11 patients with hypertrophic cardiomyopathy without a resting outflow gradient, we assessed the effects of nifedipine (10 mg orally) on echocardiographic measurements of left ventricular (LV) relaxation and diastolic filling. Control and one hour post nifedipine M-mode and two-dimensional echocardiograms were performed and the following LV parameters were measured: end-diastolic dimension, systolic shortening, isovolumic relaxation time (IVRT, time from aortic component of the second heart sound to mitral valve opening; msec), maximal fiber lengthening velocity (-VCF; circ/sec), and the percent diameter increase during the rapid filling phase (%DRF; %). Cuff systolic blood pressure fell after nifedipine from 153 to 136 mm Hg (p less than 0.05) as did diastolic pressure from 97 to 85 mm Hg (p less than 0.01). Heart rate was insignificantly increased (72 to 75/min) while end-diastolic dimension and systolic shortening were unaltered. IVRT decreased from 99 to 82 msec (p less than 0.01) and both -VCF (-4.0 to -5.0 circ/sec, p less than 0.01) and % DRF (76 to 81%, p less than 0.05) increased, suggesting more rapid relaxation and augmented filling. Thus, nifedipine improves diastolic filling dynamics in hypertrophic cardiomyopathy and therefore appears to be useful for treatment of the nonobstructive form of hypertrophic cardiomyopathy.