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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

With the correct selection of drug and patient, the calcium antagonists as a group can be remarkably effective at relatively low cost of serious side effects. Almost all side effects are dose related. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil (or diltiazem) is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine which actually has the most marked negative inotropic effect. Yet caution is required when even calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide. The most marked interaction with digoxin is that with verapamil, which may raise digoxin levels by over 50%. Combination therapy of calcium antagonists with beta-blockers is increasingly common, and is probably safest in the case of dihydropyridines. Other combinations being explored are those with angiotensin-converting enzyme inhibitors and diuretics.
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PMID:Calcium channel antagonists. Part IV: Side effects and contraindications drug interactions and combinations. 315 4

The cardiac and coronary vasodilator effects of milrinone and amrinone were compared in isolated, blood-perfused papillary muscle and sinoatrial (SA) node and atrioventricular (AV) node preparations of dogs. Milrinone (0.3-100 nmol) and amrinone (0.01-3 mumol) were administered intra-arterially. Both drugs increased the force of contraction of paced and unpaced papillary muscles and the rate of automaticity of the latter; they increased sinus rate and accelerated AV nodal conduction. However, both drugs were not homogeneously effective on cardiac variables but affected them in the following order: The force of contraction of the ventricular muscle greater than SA nodal automaticity divided by AV nodal conduction greater than ventricular automaticity. In producing these cardiac effects, milrinone was 30-60 times more potent than amrinone. Both drugs increased (coronary) blood flow in all preparations. In this respect milrinone was about ten times more potent than amrinone. As a result, milrinone can be characterized as having almost equal cardiotonic and coronary vasodilatory effects, whereas amrinone is more coronary vasodilatory than cardiotonic. These differences in cardiovascular profile may contribute to their differential salutary mechanisms in the treatment of heart failure. Both drugs induced neither AV nodal tachycardia nor ventricular arrhythmia.
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PMID:Comparative study of cardiovascular profiles of milrinone and amrinone by use of isolated, blood-perfused dog heart preparations. 357 Nov 4

The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-micrograms/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 +/- 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.
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PMID:Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease. 372 37

The effect of an acute change in blood pressure (BP) on ventricular ectopic activity and the influence of antiarrhythmic agents on this effect were examined in 24 patients. In 11 patients with premature ventricular complexes (PVCs), the BP was temporarily reduced by a sodium nitroprusside drip. In all of them the incidence of PVCs was reduced (or annihilated) by the induced hypotension. In 13 patients without ventricular ectopic activity, a metaraminol drip was given until either a PVC appeared or the systolic BP reached 200 mmHg, or symptoms appeared. In 12 cases at least one PVC appeared and in 8 of them the total number of PVCs was 13 or more, usually in the form of bigeminy. The repetition of the test following quinidine administration (serum quinidine level 1.7 +/- 0.5 ng ml-1) in 6 cases did not change this pattern, with one exception. It prevented the appearance of idioventricular accelerated rhythm in one case in whom this rhythm had been induced by the hypertension provocative test before the quinidine administration. All cases, in whom the test failed to induce more than 3 PVCs, had no cardiac problem at all. Six of the 8 cases in whom the test induced 13 or more PVCs had organic cardiac disease or palpitation. Other arrhythmias observed on BP elevation, were supraventricular extra beats, nodal escape rhythms and atrioventricular block. In one case with cardiomyopathy, the BP elevation was associated with early signs of heart failure that subsided quickly. In conclusion, acute elevation on BP may be associated with the generation of PVCs and its reduction with their reduction or disappearance.
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PMID:Acute changes in blood pressure as a cause of cardiac arrhythmias. 381 38

Calcium-channel blockers are known to have depressant effects on atrioventricular (AV) nodal conduction and myocardial contractility. Because of these known depressant effects, bepridil hydrochloride, a new, long-acting, antianginal and antiarrhythmic calcium-channel blocker, was administered intravenously to patients without heart failure to determine acute hemodynamic effects. The patients studied had normal ventricular function, were without electrocardiographic conduction disturbances and were taking no drug except sublingual nitroglycerin for at least 24 hours before bepridil infusion. The study protocol included right- and left-sided cardiac catheterization with infusion of bepridil at 2 mg/kg for 15 minutes followed by 1 mg/kg for 15 minutes in 10 patients, and infusion of bepridil at 3 mg/kg for 15 minutes followed by 1 mg/kg for 15 minutes in 8 patients. Pressures, Fick cardiac output, resistances, left ventricular (LV) dP/dt, LV stroke work index and rate-pressure product of the left ventricle were monitored. There were no significant changes during bepridil infusion at either dose for cardiac output, systemic vascular and pulmonary vascular resistances, LV stroke work index, heart rate, arterial blood pressure and rate-pressure product. There was mild depression of LV dP/dt during bepridil infusion. Further, LV end-diastolic pressure, pulmonary capillary wedge pressure and pulmonary arterial pressures were significantly increased during bepridil infusion. There were no apparent changes in AV nodal or intraventricular conduction during bepridil infusion. We conclude that bepridil appears to be a safe drug for intravenous administration despite mild depression of myocardial function in patients with normal baseline hemodynamic function who are not receiving concomitant beta-blocker therapy.
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PMID:Hemodynamic effects of intravenous bepridil in patients with normal left ventricular function. 387 53

The immediate haemodynamic and electrophysiologic effects of intravenous prenalterol 2.5-75 micrograms/kg in patients with coronary heart disease without clinical heart failure were investigated during fixed rate atrial pacing. Right ventricular peak dP/dt increased pronounced and serum concentration dependent after prenalterol concomitant with an increase in stroke volume and a moderate decrease in peripheral vascular resistance. The effects on haemodynamics after prenalterol were thus serum concentration dependent but with marked interindividual variation. AV nodal conduction velocity increased significantly. It is concluded that prenalterol possess pronounced inotropic properties. The haemodynamic response to prenalterol intravenously is to a lesser degree dependent on the chronotropic effects of the drug and it is often unpredictable.
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PMID:The immediate haemodynamic and electrophysiological response to prenalterol during fixed rate pacing in patients with chronic ischaemic heart disease. 395 93

In 67 consecutive patients with inferior wall acute myocardial infarction (AMI), 99m-technetium pyrophosphate scintigraphy was performed 36 to 72 hours after the onset of chest pain to detect right ventricular (RV) involvement. All patients were continuously monitored during at least 3 days to detect rhythm and conduction disturbances. In 29 patients RV involvement was diagnosed by scintigraphy. None of these 29 patients showed clinical signs of right-sided heart failure. Fourteen of the 19 patients showing atrioventricular (AV) nodal condution disturbances in the setting of inferior AMI also had RV involvement. Therefore, the incidence of high-degree AV nodal block in patients with RV involvement (14 of 29 patients) was 48% compared to only 13% (5 of 38) in patients with inferior AMI without RV involvement.
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PMID:Right ventricular involvement with acute inferior wall myocardial infarction identifies high risk of developing atrioventricular nodal conduction disturbances. 632 59

The haemodynamic and electrophysiologic responses to rapid intravenous injection of digitoxin (0.6 mg over 5 min) were measured in 6 patients with chronic coronary heart disease without clinical heart failure. Two minutes after end of injection peripheral resistance increased and stroke volume fell, while peak dP/dt in the right ventricle showed minimal increase. AV nodal conduction velocity decreased markedly. Thereafter, the peripheral resistance remained unchanged, stroke volume and peak dP/dt in the right ventricle increased slightly, while AV conduction remained stable. In 2 control patients stable values were found during 60 min. We conclude that digitoxin given intravenously as a single bolus injection induces an abrupt slight increase in peripheral resistance. Thereafter, a gradual increase in inotropy is found. The effect on the AV node appears rapidly and remains stable.
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PMID:Effect of intravenous digitoxin on inotropy, haemodynamics and P-Q interval in ischaemic heart disease. 648 88

Sinus nodal dysfunction (SND) and complete heart block (CHB) in congenital heart disease (CHD) are commonly associated with congestive heart failure, syncopal attacks, and sudden death. Permanent cardiac pacing (PCP) is required to avoid these manifestations which are frequently associated with a high rate of complications, particularly in the younger age group. Twenty patients with CHD aged 4 months to 46 years underwent pacemaker implantation. Twelve (60%) were less than 20 years of age. CHB was present in 15 patients: in 10 it developed 1 week to 11 years following surgery, in two it was congenital, and in three patients it developed spontaneously with previous conduction disturbances. SND was present in 5 patients: it was congenital in two patients and developed post-operatively in three. Seventeen patients are alive and no syncopal attacks or bradyarrhythmias were recorded 2.5 to 12.5 years following the initiation of PCP. Improvement in the cardiac output was noted in most patients with heart failure. The three patients who died had adequately functioning pacemakers. Only nine re-implantations were needed, seven of them in adult patients after closure of an atrial septal defect. Our experience indicates a favourable outcome for patients with CHD needing PCP.
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PMID:Permanent cardiac pacing in congenital heart disease: a follow-up study of 20 patients. 649 55


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