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Comparison of amlodipine or nifedipine treatment with developing congestive heart failure: effects on myocyte
J H McElmurray1, R Mukherjee, T M Patterson
1Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Background:
Past studies have suggested that amlodipine, a dihydropyridine L-type Ca(2+) channel antagonist, may exert useful effects in congestive heart failure (CHF). The present study examined the effects of amlodipine or nifedipine treatment in a model of developing CHF on left ventricular (LV) pump function and myocyte contractility.
Methods And Results:
Pigs (25 kg) were randomly assigned to 1 of 4 groups: 1) pacing-induced CHF (rapid atrial pacing at 240 bpm) for 3 weeks (n = 9), 2) concomitant Ca(2+) channel blockade with amlodipine (1.5 mg/kg/day) and rapid pacing (n = 7), 3) concomitant Ca(2+) channel blockade with nifedipine (0.7 mg/kg twice daily) and rapid pacing (n = 7), and 4) sham controls (n = 7). LV fractional shortening fell with pacing CHF from baseline values (17% +/- 1% v 42% +/- 1%, P <.05). With rapid pacing and concomitant amlodipine treatment, LV fractional shortening increased from pacing CHF values (24% +/- 1%, P <.05) but was unchanged with concomitant nifedipine treatment (20% +/- 2%, P =.2). LV myocyte velocity of shortening, as measured by high speed videomicroscopy, was reduced with pacing CHF compared with controls (42 +/- 2 microm/s v 87 +/- 9 microm/s, P <.05), and increased from pacing CHF values with amlodipine or nifedipine treatment (62 +/- 8 microm/s, 64 +/- 4 microm/s, respectively; P <.05). Inotropic response to extracellular Ca(2+) (8 mmol/L) was reduced with pacing CHF (94 +/- 5 microm/s v 160 +/- 15 microm/s, P <.05) and increased from CHF values with amlodipine or nifedipine treatment (132 +/- 14 microm/s and 133 +/- 7 microm/s, respectively, P <.05) CONCLUSIONS: These results suggest that the primary mechanism for the effects of amlodipine on myocyte contractility in developing CHF is because of direct Ca(2+) channel blockade.
Insights
Amlodipine improved cardiac function in a congestive heart failure (CHF) model by directly blocking calcium channels, unlike nifedipine. This study highlights amlodipine
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Congestive heart failure (CHF) is a complex cardiovascular condition.
- Dihydropyridine L-type Ca(2+) channel antagonists, like amlodipine, have shown potential in managing CHF.
- Understanding the specific mechanisms of these drugs is crucial for effective treatment.
Purpose of the Study:
- To investigate the effects of amlodipine and nifedipine on left ventricular (LV) pump function and myocyte contractility in a model of developing CHF.
- To compare the efficacy of amlodipine versus nifedipine in mitigating the detrimental effects of pacing-induced CHF.
Main Methods:
- Pigs were subjected to rapid atrial pacing to induce CHF.
- Animals were treated with either amlodipine, nifedipine, or received no treatment (sham controls).
- Left ventricular (LV) fractional shortening and myocyte contractility were assessed using echocardiography and high-speed videomicroscopy.
Main Results:
- Pacing-induced CHF significantly reduced LV fractional shortening and myocyte contractility.
- Amlodipine treatment improved LV fractional shortening and myocyte contractility in CHF pigs.
- Nifedipine treatment did not significantly improve LV fractional shortening but did enhance myocyte contractility.
- Both amlodipine and nifedipine restored the inotropic response to extracellular calcium in CHF models.
Conclusions:
- Amlodipine demonstrates beneficial effects on cardiac function in a developing CHF model.
- The primary mechanism of amlodipine's action in CHF appears to be direct calcium channel blockade.
- These findings support the potential therapeutic role of amlodipine in managing congestive heart failure.
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