Pulmonary oedema precipitated by nifedipine.

Gillmer, D J; Kark, Pieter

doi:10.1136/bmj.280.6229.1420

Cited by 103 publications

(18 citation statements)

References 4 publications

(2 reference statements)

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“…These data are similar to those reported by Hung et al,20 who used a dose of diltiazem of 360 mg/day. Since calcium-channel blockers have negative inotropic effects in vitro43 and in vivo, [1][2][3][4][5][6][7][8][9][10][11][12][13] it is clear that their interaction with /3-blockers may be hazardous, particularly in patients with a history of congestive heart failure"- [17][18][19] or with a low (less than 40%) ejection fraction.29…”

Section: Resultsmentioning

confidence: 99%

Beneficial effects of high-dose diltiazem in patients with persistent effort angina on beta-blockers and nitrates: a randomized, double-blind, placebo-controlled cross-over study.

Boden¹,

Bough²,

Reichman³

et al. 1985

Circulation

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The effects of orally administered diltiazem combined with maximally tolerated doses of /3-blockers and nitrates were assessed in 12 patients, who during stress testing exhibited persistent effort angina and continued objective evidence for inducible myocardial ischemia. Patients performed multistage semisupine exercise on a bicycle ergometer during equilibrium-gated radionuclide angiography after consecutive 2 week treatment periods of placebo or diltiazem 90 mg qid (mean dose 340 mg/day) combined with maximally tolerated propranolol (mean dose 178 mg/day) and isosorbide dinitrate (mean dose 137 mg/day). All medications (including diltiazem or placebo) were administered four times daily for the duration of the study. Diltiazem or placebo was administered according to a double-blind design, with randomized cross-over at the end of each 2 week treatment period. The average number of angina attacks decreased during the double-blind cross-over phase of the trial (7 + 7 episodes/week at baseline vs 4 ± 3 on placebo vs 2 ± 2 on diltiazem; p = .08). Angina pectoris was abolished during peak exercise in eight of 12 patients on diltiazem (p < .05 vs placebo). Diltiazem increased total exercise duration from 276 ± 92 to 310 ± 78 sec (p < .005 vs baseline). Diltiazem likewise increased the time to onset of angina from 231 ± 84 sec at baseline to 305 ± 77 sec (p < .005), as well as the time to the onset of 1 mm ischemic ST segment depression (p = .0 1). Diltiazem decreased heart rate at rest, during submaximal workload, and at peak exercise (p < .05), and decreased systolic blood pressure at peak exercise only (p < .05). A significant decline in rate-pressure product at submaximal and peak exercise was noted (p < .05). At any given workload there was significantly less ST segment depression during submaximal (p = .05) and peak exercise (p < .025). No difference was noted in mean left ventricular ejection fraction during placebo or diltiazem therapy at rest and during peak exercise. The effect of adding high-dose diltiazem to maximally tolerated doses of isosorbide and propranolol in improving exercise tolerance and reducing maximal ST segment depression suggests an attenuation of myocardial ischemia. A reduction in rate-pressure product at submaximal and peak workload indicates that patients can perform a higher degree of external work before the onset of ischemia. Thus the principal mechanism for the observed improvement in myocardial ischemia with diltiazem in patients with persistent effort angina in spite of maximally tolerated doses of ,Bblockers and nitrates appears to be a further incremental decrease in myocardial oxygen demand, although the decrease in heart rate may have facilitated an improvement in myocardial oxygen supply. Circulation 71, No. 6, 1197-1205, 1985

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Section: Resultsmentioning

confidence: 99%

Beneficial effects of high-dose diltiazem in patients with persistent effort angina on beta-blockers and nitrates: a randomized, double-blind, placebo-controlled cross-over study.

Boden¹,

Bough²,

Reichman³

et al. 1985

Circulation

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“…Although nifedipine has been used in pulmonary edema [4], in some cases heart failure can be induced or pre cipitated [5,6]. In 1 such patient, concom itant use of calcium channel blocker with beta-blocker precipitated congestive car diac failure [5], whereas in another case pulmonary edema was induced by nifedi pine in a patient with fixed outflow tract obstruction due to aortic stenosis [6]. To our knowledge, pulmonary edema due to nifedipine in primary pulmonary hyper tension has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Edema with Nifedipine in Primary Pulmonary Hypertension

Batra

Segall

Ahmed³

1985

Respiration

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Despite occasional case reports, vasodilator therapy of primary pulmonary hypertension remains unsatisfactory. Nifedipine, a calcium channel antagonist, has recently been recommended for the treatment of primary pulmonary hypertension. Transient mild side effects to this drug have been known. In this report we describe a case of primary pulmonary hypertension in whom oral nifedipine use was followed by fatal pulmonary edema. We suggest that nifedipine has the potential of causing life-threatening complications of pulmonary edema in patients with severe primary pulmonary hypertension, and in this condition it should be used cautiously.

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“…Although the initial experience with the use of nifedipine in CHF led some investigators to conclude [10][11][12][13][14][15][16][17] that the negative inotropic effect of nifedipine could be offset by its vasodilatory effect, further evaluation in larger groups of patients demonstrated the clinical relevance of the cardiodepressant effect of the drug [18][19][20][21]. Comparison of nifedipine with nitroprusside [22] demonstrated a smaller augmentation in cardiac output and a larger decrease in systemic blood pressure with nifedipine despite a similar reduction in SVR.…”

Section: Clinical Experience With Calcium Antagonists In Heart Failurementioning

confidence: 99%

Calcium Channel Blockers in Heart Failure

Elkayam

1998

Cardiology

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A considerable effort has been made in the last 15 years to evaluate the safety and efficacy of calcium channel blockers (CCBs) in the treatment of patients with chronic congestive heart failure (CHF). Available studies have provided strong evidence for a potential detrimental effect of the first-generation calcium antagonists in patients with CHF, indicating the need for great caution when these drugs are used in patients with significant depression of left ventricular systolic function. A number of second-generation CCB have demonstrated a strong vasodilatory effect and favorable hemodynamic action but failed to show a similar improvement in exercise capacity, morbidity and mortality. Moreover, drugs such as nicardipine and nisoldipine have resulted in a detrimental effect in some patients and, therefore, cannot be considered safe when used in patients with moderate-to-severe heart failure. Available information from the V-HeFT III study demonstrate a lack of an unfavorable effect of felodipine on exercise tolerance in patients with chronic heart failure. Although mortality rate was similar in both the felodipine and the placebo group, because of the relatively small number of patients in this study, no clear conclusion can be drawn regarding the effect of felodipine on mortality in patients with CHF. An encouraging signal regarding a potential role of CCB in the treatment of chronic heart failure has been provided by the recently completed PRAISE study. This prospective large-scale study demonstrated the safety of amlodipine, a long-acting dihydropyridine derivative, when used in patients with heart failure due to coronary artery disease. Furthermore, this study demonstrated a substantial reduction in mortality in patients with CHF due to nonischemic cardiomyopathy and provided a strong indication for a potential therapeutic benefit of amlodipine when added to standard CHF therapy in this patient population. No clear explanation is available at the present time regarding the reason for the deleterious effect demonstrated with some of the dihydropyridines and the contrasting benefit seen with amlodipine. Finally, more information regarding the safety and efficacy of dihydropyridines should become available in the next year. The PRAISE II study is ongoing and will provide further information regarding the therapeutic role of amlodipine in patients with nonischemic dilated cardiomyopathy. The MACH-1 study is evaluating the effect of mibefradil, a predominant T-type channel blocker with an ideal activity profile, on morbidity and mortality in patients with chronic CHF.

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Pulmonary oedema precipitated by nifedipine.

Cited by 103 publications

References 4 publications

Beneficial effects of high-dose diltiazem in patients with persistent effort angina on beta-blockers and nitrates: a randomized, double-blind, placebo-controlled cross-over study.

Beneficial effects of high-dose diltiazem in patients with persistent effort angina on beta-blockers and nitrates: a randomized, double-blind, placebo-controlled cross-over study.

Pulmonary Edema with Nifedipine in Primary Pulmonary Hypertension

Calcium Channel Blockers in Heart Failure

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