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Oral nifedipine in the long-term management of severe chronic heart failure
Insights
Nifedipine improved heart function and symptoms in patients with chronic heart failure. These hemodynamic benefits, including increased cardiac index, were sustained with long-term therapy but lost upon discontinuation.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Chronic heart failure (CHF) is a debilitating condition with limited treatment options.
- Idiopathic cardiomyopathy contributes significantly to refractory heart failure.
- Evaluating novel therapeutic agents for CHF is crucial.
Purpose of the Study:
- To assess the hemodynamic effects of nifedipine in patients with symptomatic chronic refractory heart failure.
- To determine the sustained efficacy and tolerability of nifedipine therapy.
- To investigate the reversibility of nifedipine's effects upon discontinuation.
Main Methods:
- A study involving 10 patients with symptomatic chronic refractory heart failure.
- Hemodynamic parameters were measured before and during nifedipine treatment.
- Repeat assessments were conducted at 2 months and after drug discontinuation.
Main Results:
- Nifedipine significantly increased cardiac index, stroke volume index, and stroke work index.
- Nifedipine significantly reduced left ventricular filling pressure, blood pressure, pulmonary arterial pressure, and vascular resistance.
- Symptomatic improvement (at least one NYHA class) was observed in all patients, with sustained effects at 2 months.
Conclusions:
- Nifedipine demonstrates significant hemodynamic benefits in severe chronic heart failure.
- Long-term nifedipine therapy is well-tolerated and leads to sustained symptomatic improvement.
- The hemodynamic benefits of nifedipine are reversible upon discontinuation, highlighting its potential for ambulatory therapy.
Abstract:
We evaluated the hemodynamic effects of nifedipine in 10 symptomatic patients with chronic refractory heart failure due to idiopathic cardiomyopathy. Nifedipine significantly increased cardiac index (from 1.80 +/- 0.4 to 3 +/- 0.6 L/min/m2), stroke volume index (from 21 +/- 6 to 33 +/- 8 ml/beat/m2), and stroke work index (from 17.9 +/- 7 to 25.5 +/- 7 g-m/m2). The drugs also produced a significant decrease in left ventricular filling pressure (from 24.6 +/- 3 to 19 +/- 2 mm Hg), mean blood pressure (from 86 +/- 9 to 74 +/- 5 mm Hg), mean pulmonary arterial pressure (from 31.9 +/- 5 to 25.6 +/- 3 mm Hg), total systemic vascular resistance (from 2,104 +/- 329 to 1,088 +/- 249 dyn/s/cm-5), and pulmonary vascular resistance (from 200 +/- 71 to 107 +/- 50 dyn/s/cm-5). Heart rate remained unchanged. In all patients maintained on nifedipine therapy, repeat hemodynamic studies at 2 months revealed sustained effects, and all patients had symptomatic improvement of at least one New York Heart Association (NYHA) functional class. Long-term treatment was well tolerated. Forty-eight hours after discontinuation of nifedipine administration the hemodynamic benefits were lost. We conclude that nifedipine may be of value for long-term ambulatory therapy of severe chronic heart failure.