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

Thirty-two patients with chronic heart failure were investigated with radionuclide ventriculography at rest and during exercise. The global ejection fraction (EF), ejection rate, ejection time, and filling rate were measured. The patients were subdivided into three subgroups: patients with extremely (< 25%), moderately (25-33%), and mildly decreased EF (33-40%). All patients were investigated by thallium-201 myocardial scintigraphy and the correlation between ejection parameters and infarct size was investigated. In a random protocol 17 patients (14 men, 3 women, mean age of 54.6 years) received beta-acetyldigoxin at a dose of 0.3 mg daily over 4 weeks, 15 patients (13 men, 2 women, mean age of 58.2 years) received nisoldipine at a dose of 20 mg daily. Patients on digitalis showed a further lowering of the extremely decreased EF (-1%), but in patients with moderately decreased EF, digoxin produced a marked increase in EF of +8% (p < 0.001). In mildly decreased EF, there was no significant change (+0.3%, n.s.). Nisoldipine produced an increase in pump function (+2%) in the group with extremely decreased EF up to 9% in some individual cases. A significant increase (+5%) was achieved in moderately decreased EF, while patients with mildly decreased EF did not respond. Thus, nisoldipine may be indicated in the treatment of heart failure after repeated myocardial infarctions, in particular in patients with severely decreased ejection fraction.
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PMID:Effects of calcium antagonists in patients with coronary disease and heart failure: left ventricular function following nisoldipine measured by radionuclide ventriculography. 128 15

The effects of the second generation calcium channel blocking drug nisoldipine on subjective and objective measurements of exercise performance were studied in 19 patients with moderate to severe heart failure (9 New York Heart Association functional class 2, 9 class 3 and 1 class 4) due to fixed ventricular dysfunction following myocardial infarction. Nisoldipine (10 mg 3 times daily) or placebo were administered for 8 weeks in a double-blind parallel study, assessing exercise performance by symptom-limited treadmill exercise testing using a modified Naughton protocol. Nisoldipine was well-tolerated and produced a small increase in peak estimated workload performed (6.2 +/- 2.9 to 8.2 +/- 3.0 METs, p = 0.06). The rate of perceived exertion (Borg scale) increased from 17.5 +/- 2.2 to 18.8 +/- 1.2 (p less than 0.02). The higher workload was performed at a lower peak systolic blood pressure (p = 0.03), higher peak heart rate (p = 0.06) and identical double product (NS). There was no change in resting and peak heart rate and blood pressure or in exercise performance in patients receiving placebo. Resting left ventricular ejection fraction, measured by radionuclide ventriculography, was unchanged after 8 weeks both in the placebo (21 +/- 9 to 20 +/- 9%) and nisoldipine (34 +/- 17 to 36 +/- 19%) groups.
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PMID:Effect of nisoldipine on exercise performance in heart failure following myocardial infarction. 177 13

To study the haemodynamic and neurohumoral effects of nisoldipine (2 X 10 mg) vs captopril (3 X 25 mg), 24 patients with heart failure (New York Heart Association class II and III) due to coronary artery disease were treated in a randomized double-blind trial over 3 months. Both drugs were well tolerated. Clinical status was similarly improved in both groups, nisoldipine exerted an additional antiischaemic effect. Nisoldipine lowered the mean arterial pressure and capillary wedge pressure acutely and also after long-term treatment. The increase in cardiac index and stroke volume index, however, which was pronounced after acute administration, was no longer present after 3 months of therapy at rest and was abolished during exercise. Norepinephrine plasma concentration increased after the first dose, plasma renin activity did not change, and aldosterone plasma concentration showed a small insignificant decrease. Urine concentrations of norepinephrine and vasopressin were slightly elevated after the 3-month therapy. After captopril, mean arterial pressure and pulmonary capillary wedge pressure decreased acutely and at follow up. Cardiac index and stroke volume index increased significantly only during exercise at follow-up. Plasma renin activity was significantly elevated and aldosterone plasma concentration only slightly lowered. In contrast to what was seen with nisoldipine, plasma norepinephrine concentration and urine catecholamine and vasopressin concentrations remained unchanged. In conclusion, the pronounced haemodynamic effects seen after the first dose of nisoldipine are mostly abolished after long-term treatment, probably due to neurohumoral counterregulation. The haemodynamic response to captopril is complete only after long-term treatment, without evidence of activation of the neurohumoral systems.
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PMID:Acute and long-term haemodynamic and neurohumoral response to nisoldipine vs captopril in patients with heart failure: a randomized double-blind study. 168 8

We studied the acute effects of the calcium antagonist nisoldipine in 10 conscious pigs with chronic heart failure. Left ventricular dysfunction was induced by permanent ligation of the left circumflex coronary artery. Two to three weeks after myocardial infarction the effects of four consecutive 10 min intravenous infusions of nisoldipine (0.05; 0.1; 0.25 and 0.5 micrograms kg-1 min-1) or its solvent on systemic haemodynamics were evaluated. In addition, we used the radioactive microsphere technique to study the distribution of cardiac output after each dose of nisoldipine. Nisoldipine significantly (P less than 0.05) increased heart rate (from 144 +/- 9 to 161 +/- 8 beats min-1), cardiac output (from 2.1 +/- 0.1 to 2.9 +/- 0.2 l min-1), stroke volume (from 14 +/- 1 to 18 +/- 1 ml) and left ventricular dP/dtmax (from 2600 +/- 100 to 3500 +/- 250 mmHg s-1), but had no effect on arterial blood pressure. Left ventricular end-diastolic pressure (from 19 +/- 2 to 16 +/- 1 mmHg) and systemic vascular resistance (from 52 +/- 3 to 37 +/- 3 mmHg min l-1) decreased after nisoldipine. The nisoldipine-induced increase in cardiac output did not affect blood flow to the kidneys, brain, liver or skin, but perfusion of the stomach (84%), adrenals (84%) and normal myocardium (from 200 +/- 25 to 321 +/- 38 ml min-1 100 g-1) as well as infarcted myocardium (from 41 +/- 8 to 61 +/- 19 ml min-1 100 g-1) increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nisoldipine improves blood flow to skeletal muscles in conscious pigs with chronic heart failure. 235 Nov 64

The acute hemodynamic effects of intravenous nisoldipine were studied in 10 patients with severe congestive heart failure. Nisoldipine was administered in three consecutive doses (1.5, 3.0, and 6.0 micrograms/kg) at least 150 min apart. Following the first dose, mean arterial pressure declined from 96 +/- 17 to 87 +/- 16 mm Hg (p less than 0.01), cardiac index increased from 2.1 +/- 0.7 to 2.4 +/- 0.7 L/min/m2 (p less than 0.025), and systemic vascular resistance fell from 27 +/- 10 to 19 +/- 6 units (p less than 0.01). Maximal hemodynamic effects occurred by 2 to 5 min and gradually waned over the next 120 min. There were no significant changes in heart rate or filling pressures. The time course for the hemodynamic effects were similar with subsequent doses but the magnitude of change was significantly greater. There was a dose-dependent increase in peak arterial nisoldipine concentration. Baseline plasma norepinephrine and renin were high but did not change with nisoldipine administration. No significant changes were seen after nisoldipine administration. No major side effects were observed. These data suggest that nisoldipine is a potent arterial vasodilator that can be of benefit in patients with low output cardiac failure.
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PMID:Intravenous nisoldipine in severe congestive heart failure. 245 47

The effect of intravenous nisoldipine (0.12 microgram/kg/min) on diastolic left ventricular (LV) dysfunction was studied from simultaneous hemodynamic and radionuclide measurements in 12 patients with New York Heart Association class II to IV cardiac failure. The initial LV filling fraction was low, the peak LV filling rate normalized for end-diastolic volume was decreased, and the pulmonary capillary wedge pressure (PCWP) was high and associated with clinical shortness of breath. Nisoldipine produced an increase in LV filling fraction from 36 +/- 17% to 43 +/- 20% (p = 0.003). The increase in filling took place in both early and late diastole: peak early filling rate (PFR) increased in 11 of the 12 patients (p = 0.02) and late diastolic filling rate (atrial [A] wave in eight of them (NS). When the determinants of these changes, were examined further, it was found that in the control state PFR was inversely related to LV end-systolic volume (r = 0.77), whereas the A wave was related in exponential fashion to PCWP (preload) (r = 0.79). Nisoldipine did not change the slope of these relationships, and it did not alter the end-diastolic pressure-volume relationship, implying that inherent myocardial relaxation and distensibility were unaltered by the drug. In summary, nisoldipine improved measurements of diastolic LV dysfunction in patients with cardiac failure. This study illustrates the importance of considering ventricular loading conditions when analyzing and interpreting measurements of diastolic ventricular dysfunction. The measured changes in diastolic LV function during infusion of nisoldipine appear to be due to alterations in ventricular loading conditions rather than to a direct myocardial effect of the drug.
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PMID:Effect of the second-generation calcium channel blocking drug nisoldipine on diastolic left ventricular dysfunction in heart failure. 277 71

We studied the acute effects of nisoldipine, a new second-generation calcium channel-blocking drug, on cardiac hemodynamics and left ventricular (LV) contractility in 10 patients with grade 2 to 4 cardiac failure. Pressures were measured from an arterial line and a flow-guided catheter in the pulmonary artery, cardiac output by thermodilution, and LV ejection fraction simultaneously by radionuclide ventriculography. Ventricular loading conditions were altered by sublingual nitroglycerin to facilitate construction of LV end-systolic pressure (radial stress)-volume and stress-shortening curves. Nisoldipine, given by continuous intravenous infusion (0.12 micrograms/kg/min), reduced mean arterial pressure (p = 0.001), systemic vascular resistance (p less than 0.05), and the double product, a measurement of myocardial oxygen demand (p less than 0.01). Cardiac index, stroke index, and LV ejection fraction increased in 8 of the 10 patients. LV contractility was initially greatly reduced and was unchanged or slightly decreased during the administration of nisoldipine. Emax, the slope of the end-systolic pressure-volume curve, was unaltered in half of the patients and decreased in the others (NS), whereas the end-systolic stress-shortening curve did not change. In summary, nisoldipine has a potentially useful acute hemodynamic profile in patients with cardiac failure; it increases forward blood flow in most patients, decreases the determinants of myocardial oxygen demand, and produces little measurable changes in the inotropic state of the left ventricle.
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PMID:Effect of the second-generation calcium channel blocker nisoldipine on left ventricular contractility in cardiac failure. 337 41

In a placebo controlled double-blind study including 10 patients with heart failure the nisoldipine/digoxin interaction was studied. Nisoldipine was shown to elevate digoxin plasma concentrations significantly by about 15% (trough levels). During chronic combination therapy with nisoldipine trough levels and plasma concentrations 4 h after the morning dose of digoxin were 1.35 +/- 0.14 and 1.92 +/- 0.16 ng ml-1 respectively, whereas they averaged to 1.16 +/- 0.14 and 1.52 +/- 0.16 ng ml-1 with digoxin and placebo (P less than 0.05; mean +/- s.e. mean). Systolic time intervals were significantly altered by nisoldipine co-administration compared with digoxin plus placebo. In certain patients the elevation of digoxin plasma levels due to nisoldipine co-administration could be of clinical relevance.
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PMID:Influence of nisoldipine on haemodynamic effects and plasma levels of digoxin. 353 Mar 3

This article examines trials of the use of two types of drugs in the treatment of myocardial infarction: angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists. ACE inhibitors are an established treatment for hypertension and heart failure and have been shown to reduce mortality from heart failure and after myocardial infarction. Six large studies have been carried out. In 1 in which an ACE inhibitor was given 3-16 days after infarction in patients with an ejection fraction < 40%, mortality was reduced by 17%. In a second study of patients who had evidence of heart failure and were followed up for 15 months, treatment with ACE inhibitors was given 3-10 days after myocardial infarction and mortality was reduced by 27%. Two other studies of 11,000 and 50,000 unselected patients with myocardial infarction showed only marginal clinical benefit. Calcium antagonists were introduced to treat hypertension and angina pectoris. In trials with patients with heart failure, the results have not been encouraging, and in some patients these agents seem to be harmful. Recently, long-acting calcium antagonists have become available, and these may avoid the deleterious effects of short-acting drugs. Since calcium antagonists act on smooth muscle, they may increase myocardial blood flow to improve function after "stunning" or "hibernation." This idea was investigated with a long-acting dihydroyridine calcium, antagonist in a randomized double-blind, placebo-controlled study (Doppler Flow, Echocardiography, and Functional Improvement Assessment of Nisoldipine Therapy-I--DEFIANT I), and a further study is being carried out. At present the widespread use of calcium antagonists after infarction is not recommended.
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PMID:Angiotensin-converting enzyme inhibitors and calcium antagonists after acute myocardial infarction. 772 23

The effects of the long-acting dihydropyridine calcium antagonist nisoldipine coat core (CC) have been investigated in > 3,500 patients with angina pectoris, hypertension, and ischemic ventricular dysfunction. In patients with angina pectoris, nisoldipine CC improved total treadmill exercise duration (p = 0.027), delayed the onset of angina pectoris (p = 0.009), and increased time to exercise-induced ST-segment depression (p = 0.061). In general, nisoldipine 20-40 mg was effective, and the dose-response curve flattened thereafter. In patients with hypertension, 10-40 mg once daily as monotherapy reduced blood pressure (p < 0.05), with a fall in diastolic pressure of > or = 10 mm Hg or a final diastolic pressure of < 90 mm Hg in 35-63% of patients. In most patients followed for a year, nisoldipine CC was continued as monotherapy. Efficacy was similar in patients < 65 and > 65 years of age. In the Doppler Flow and Echocardiography in Functional Cardiac Insufficiency: Assessment of Nisoldipine Therapy (DEFIANT-I) study of patients recovering from myocardial infarction, nisoldipine CC had a salutary effect on diastolic ventricular function, with a higher transmitral early filling velocity and shorter isovolumic relaxation time than in patients receiving placebo. Bicycle exercise capacity was greater (by 12 W; 95% confidence interval, 0.8-23.3) and exercise-induced ischemia occurred less frequently. The nisoldipine CC data pool (3,679 patients) showed that the drug was well tolerated with a low incidence of side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy and safety of nisoldipine coat core in the management of angina pectoris, systemic hypertension, and ischemic ventricular dysfunction. 772 25


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