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Biomedical subjects

W Kiowski

Publications and source records attributed to W Kiowski.

At least 145 records · Page 8Linked to original sources
PubMed1988

Heart valve replacement with St. Jude Medical valve prosthesis. Long-term experience in 743 patients in Switzerland.

Between November 1978 and June 1986, 828 St. Jude Medical valves were implanted in 743 patients whose mean age was 57 years (range, 1-83 years) and who had been admitted to the University Hospitals in Basel, Berne, and Lausanne, Switzerland. Aortic valve replacement was performed in 456 patients, mitral valve replacement in 200, tricuspid valve replacement in six, double valve replacement in 77, and triple valve replacement in four. In 187 patients, additional surgical interventions were performed. Operative mortality was 1.6%, and the 4-week postoperative mortality was 4.0%. During a mean follow-up period of 2.6 years, the annual mortality rate was 3.1%, and the annual cardiac mortality rate was 2.1%. The thromboembolic rate per 100 patient-years was 1.3 after aortic valve replacement, 3.0 after mitral valve replacement, and 1.0 after multiple valve replacement. The incidence of major bleeding was 1.3 per 100 patient-years. Valve dysfunction attributable to thrombotic obstruction occurred in three patients, and that attributable to leaflet dislocation in one (annual dysfunction rate, 0.2%). Twelve patients developed infectious endocarditis, six of whom died. However, in four patients, reoperation and, in two patients, antibiotic treatment alone were successful in treating the infection. A paravalvular leak necessitating reoperation developed in 10 patients. In three patients, the leak was caused by infectious endocarditis. Reoperation had no operative mortality. In three patients (0.4%), a mild hemolytic anemia was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Arterial vasodilator, systemic and coronary hemodynamic effects of nisoldipine in congestive heart failure secondary to ischemic or dilated cardiomyopathy.

The systemic and coronary hemodynamic and neurohumoral effects of nisoldipine, a calcium antagonist drug with high vascular specificity, were investigated in 17 patients with chronic congestive heart failure (CHF). Brachial artery infusions (n = 9) decreased forearm vascular resistance in a dose-dependent manner, attesting to its powerful arterial vasodilator properties. A dose of 3 micrograms/kg intravenously decreased mean blood pressure 16% and systemic vascular resistance 33%, while increasing stroke index 19% and ejection fraction 21% at rest and similarly during exercise. Pulmonary capillary wedge pressure decreased significantly during exercise. Intravenous infusion of nisoldipine increased rest coronary sinus flow 10% (p less than 0.05, n = 7), decreased rest and exercise coronary vascular resistance 28% and 19% (p less than 0.01) and rest myocardial oxygen consumption 14% (p less than 0.05). In 13 patients similar systemic hemodynamic results were found after treatment with oral nisoldipine, 2 X 20 mg for 4 weeks. Stroke index and stroke work index increased long-term more than acutely (31% and 12.4% vs 19% and 4.5% at rest, both p less than 0.05), which may indicate a compensated mild cardiodepressant effect of intravenous nisoldipine. Changes in forearm vascular resistance after intra-arterial administration did not correlate with changes of systemic vascular resistance after intravenous administration, suggesting that factors other than vascular calcium entry blockade importantly influence hemodynamic responses. Elevated control plasmas norepinephrine and renin levels, on average, did not change during chronic therapy but individual changes were compatible with a reduction of sympathetic activity in patients with hemodynamic improvement.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Calcium antagonist induced vasodilation in peripheral, coronary and cerebral vasculature as important factors in the treatment of elderly hypertensives.

Increased arteriolar tone is the pathophysiological hallmark of essential hypertension and is determined by the intracellular free calcium concentration in the vascular smooth muscle cell. Calcium influx is an important determinant of vasoconstriction and excess calcium influx-dependent vasoconstriction has been shown by plethysmographical studies in patients with essential hypertension. Calcium antagonists acutely lower BP by reducing calcium influx, calcium concentration and peripheral resistance. The degree of the attendant sympathetic nerve reflex activation and counter-regulatory mechanisms determines the antihypertensive response of the individual. Chronic monotherapy with a calcium antagonist results in an antihypertensive response, which is directly related to the patient's age and pretreatment BP and indirectly related to plasma renin levels. The resulting reduction in after-load neither leads to reduced cerebral blood flow in hypertensive patients, nor aggravates congestive heart failure. Calcium antagonists are a useful alternative to diuretics, primarily in older patients with low renin levels, either alone or combined with any other antihypertensive drug, and provide effective and safe control of blood pressure.

Aged↗
PubMed1987

Age and antihypertensive response to calcium antagonists.

Calcium antagonists are being increasingly used for the treatment of hypertension. Analysis of response patterns shows that they are particularly effective in older, low-renin and black patients. Although the reasons for this pattern are not quite clear there is evidence that the attenuated cardiovascular reflex responses may be important in these groups. Baroreflex responses are blunted in older subjects and even more so in older hypertensive patients. Patients with low-renin hypertension also show impaired sympathetic nervous system response and black subjects often have low renin levels. A diminished counter-regulatory response to the vasodilating effects of calcium antagonists may partly explain the good clinical responses of older, low-renin and black patients.

Aged↗
PubMed1987

Acute hemodynamic effects of MDL 19205 in mild congestive heart failure.

MDL 19205 4-ethyl-1-,3-dihydro-5-(4-pyridinylcarbonyl)-2H-imidazol-2-one, a new cardioactive agent, has been shown to increase myocardial contractile force in animals. It is effective by both oral and intravenous routes. We studied 11 patients with congestive heart failure--in 10 cases owing to coronary artery disease, and in one to cardiomyopathy. All patients had symptoms of NYHA class II or III, left ventricular ejection fractions (LVEF) less than 55%, and left ventricular end-diastolic pressures (LVEDP) greater than 15 mm Hg. Following routine coronary angiography and ventriculography, 0.5 mg/kg MDL 19205 was administered intravenously over 5 min to six patients. Thirty minutes after injection, hemodynamic measurements and ventriculography were repeated. Mean LVEF increased from 42 to 49% (p less than 0.05 for baseline vs. 30 min). In five patients ventriculography was repeated 60 min after placebo administration: LVEF decreased from 45 to 40%. LVEDP decreased from 29 +/- 8 to 16 +/- 8 mm Hg after MDL 19205 administration (p less than 0.05) and remained constant at 24 mm Hg in the placebo group. The small although nonsignificant increase of LVdP/dt after MDL 19205 administration (10 +/- 33%), together with a considerable decrease in LVEDP, was consistent with a positive inotropic effect. LVdP/dt/total pressure developed (VPM), a measure of contractility relatively independent of changes in pre- and afterload, increased from 1.0 +/- 0.3 to 1.3 +/- 0.3 s-1 (p less than 0.05). Neither parameter of contractility (LVdP/dt and VPM) changed significantly in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiotonic Agents↗
PubMed1987

The vasodilator potency of atrial natriuretic peptide in man.

The vasodilating potency of alpha-human atrial natriuretic peptide (alpha-hANP) was investigated in the forearms of 16 normotensive subjects, 22 to 48 (mean 28) years old, with the use of venous occlusion plethysmography. alpha-hANP, 0.005 to 1.5 micrograms/min/100 ml forearm volume (FAV), infused in nine dose steps into the brachial artery increased forearm blood flow (FAF; ml/min/100 ml FAV) from 2.8 +/- 0.4 (SEM) to a maximum of 9.6 +/- 1.1. Forearm vascular resistance (mean arterial pressure/FAF) decreased by 72%. The alpha-hANP dose that produced a 50% vasodilator response was 0.093 +/- 0.016 microgram/min/100 ml FAV (n = 11) and it resulted in a venous plasma concentration of ANP (pANP) of 115 +/- 7 pmol/liter (normal 2 to 80; radioreceptor assay). Intraindividually, the maximum dose of alpha-hANP induced an increase in FAF that was 60% of the maximum response to sodium nitroprusside (14.1 +/- 1.8). Combined infusions (n = 9) of maximum forearm vasodilator doses of alpha-hANP and nitroprusside increased FAF to 22.7 +/- 3.4; this additive vasodilator effect of alpha-hANP and nitroprusside is consistent with their different actions on the guanylate cyclase system. In man, the direct vasorelaxant effect of alpha-hANP occurs at concentrations within the upper normal range of pANP, suggesting a physiologic vasodilator role for alpha-hANP.

Adult↗
PubMed1987

Mechanisms of action of calcium antagonists in hypertension.

Cytosolic free calcium concentrations determine the magnitude of tension development of smooth muscle cells and are pivotal for regulation of vascular smooth muscle tone and systemic vascular resistance. Elevated free calcium concentrations have been found in platelets from hypertensive patients, and platelet free calcium concentration, possibly an index of vascular smooth muscle cell free calcium concentration, correlated with blood pressure in normotensive and hypertensive subjects. Increased systemic vascular resistance in essential hypertension depends on increased calcium influx. Calcium antagonists lower cytosolic free calcium concentrations mainly through a reduction of transmembraneous calcium influx and are potent arterial vasodilators. High blood pressure is lowered through a reduction of elevated systemic vascular resistance but, in contrast to other direct acting vasodilators, without clinically relevant sympathetic reflex activation. However, subtle changes of sympathetic nervous system activity may codetermine the acute and chronic blood pressure response. Calcium antagonists do not lead to volume retention, because of improved intrarenal hemodynamics and a diuretic effect. Interference with angiotensin and sympathetically mediated vasoconstrictor mechanisms probably also contributes to their antihypertensive effects. This favorable hemodynamic profile renders calcium antagonists suitable for monotherapy of uncomplicated hypertension where they are particularly effective in older patients and also for the therapy of hypertensive crisis.

Blood Platelets↗
PubMed1987

Greater vasodilator responsiveness to atrial natriuretic peptide in low-renin essential hypertensives.

Forearm vasodilator responses to atrial natriuretic peptide (ANP) were studied in twelve untreated patients with essential hypertension and twelve normotensive subjects. Alpha-human ANP (0.005 to 1.5 micrograms/min per 100 ml forearm volume) infused into the brachial artery increased forearm blood flow dose-dependently. This was paralleled by a decrease in forearm vascular resistance (FVR) which, at lower doses, was greater in essential hypertensives than in normotensives (P less than 0.001), and showed a lower ED50 for ANP in essential hypertensives (P less than 0.01). At higher doses of ANP the difference in vasodilator response between hypertension and normotension disappeared; the response to ANP was associated with a fall (P less than 0.01) in systemic blood pressure in hypertensives but not normotensives. At lower doses, the decreases in FVR were correlated directly with plasma renin activity in hypertensives (r = 0.656; P less than 0.05) but not normotensives. These data suggest greater vasodilator responsiveness to infusions of low doses of ANP in essential hypertensives, which is greater in low-renin states and blunted in high-renin states.

Adult↗
PubMed1987

Calcium antagonists in hypertension.

Calcium antagonists are potent arterial vasodilators with no long-term effect on sympathetic reflex activity or sodium and volume retention. This favourable haemodynamic profile makes them suitable for monotherapy of hypertension, where they act to reduce an enhanced, calcium-influx-dependent vasoconstrictor mechanism which may be brought about by altered smooth-muscle cation handling and increased intracellular concentrations of free calcium. Clinical studies have proved the efficacy, safety and acceptability of calcium antagonists alone or in combination with other drugs in uncomplicated hypertension; calcium antagonists are particularly effective in older patients, those with low renin levels and, possibly, black patients. These properties and the efficacy of calcium antagonists in the treatment of severe and accelerated hypertension or hypertensive emergencies make them a valuable addition to the drugs already available for the treatment of hypertension.

Animals↗
PubMed1987

Bolus injection of cimetidine and hypotension in patients in the intensive care unit. Incidence and mechanisms.

Incidence and mechanisms of cimetidine-induced hypotension were investigated during the first intravenous injection of cimetidine (200 mg over three minutes) in 68 consecutive patients in the intensive care unit. Systolic pressure decreased more than 5 mm Hg (average, 14 mm Hg) in 50 patients, exceeding 30 mm Hg in nine (13%), while heart rate and pulmonary artery pressure (seven patients) did not change. Blood pressure decreased significantly more in patients requiring vasoconstrictor drug support. The arterial vasodilator properties of cimetidine were demonstrated in 12 normal volunteers in whom brachial artery cimetidine infusions caused a significant decrease of forearm vascular resistance. This effect was more pronounced when forearm vessels were preconstricted with dopamine hydrochloride (n = 6) or norepinephrine (n = 6), pointing toward an interference of cimetidine with sympathetically mediated vasoconstriction. Thus, intravenous injection of cimetidine in critically ill patients, presumably through arterial vasodilatation, is frequently associated with decreases of blood pressure, particularly in patients requiring vasoconstrictor drug support.

Adolescent↗
PubMed1986

Calcium antagonists and the second drug for hypertensive therapy.

Calcium antagonist monotherapy is more effective in older patients and in those with low plasma renin activity, whereas beta blockers control blood pressure better in younger patients and in those with normal or high renin activity. Monotherapy with a calcium antagonist has been shown to result in the reduction of diastolic blood pressure to equal to or less than 95 mm Hg in more than 80 percent of patients with essential hypertension. We investigated the antihypertensive efficacy of verapamil plus an angiotensin converting enzyme inhibitor and nifedipine plus a beta blocker in 24 patients (aged 41 to 68) with moderate to severe hypertension in whom monotherapy with a calcium antagonist had been ineffective. Blood pressure recorded in patients during the placebo period was 175 +/- 3/111 +/- 2 mm Hg (mean +/- SEM). Twelve patients received monotherapy with nifedipine (50.0 +/- 5.2 mg per day) and 12 others received verapamil (460 +/- 20 mg per day); neither treatment resulted in the reduction of diastolic blood pressure to less than 90 mm Hg. However, this goal was achieved when atenolol (89.5 +/- 25.7 mg per day) was added to the regimen of patients receiving nifedipine and enalapril (29.5 +/- 5.0 mg per day) was added to the regimen of those receiving verapamil; resultant blood pressures were 127 +/- 3/83 +/- 2 mm Hg and 137 +/- 5/85 +/- 1 mm Hg, respectively. It is suggested that in patients in whom hypertension is inadequately controlled by calcium antagonist monotherapy, counter-regulatory mechanisms can be blocked by the addition of a beta blocker or an angiotensin converting enzyme inhibitor to the calcium antagonist regimen, resulting in greatly improved, simple, well-tolerated, and safe control of blood pressure.

Adrenergic beta-Antagonists↗
PubMed1986

[Secretion of atrial natriuretic peptide: relation to atrial pressure and systemic blood pressure].

To determine the influence of atrial pressure, heart rate and loss of atrial-ventricular synchrony in the release of atrial natriuretic peptide (ANP), plasma ANP concentrations were measured by radio-receptor assay in 12 patients during diagnostic cardiac catheterization and in patients with atrial fibrillation and during cardiac pacing. There was a relationship between right atrial pressure and right atrial ANP concentration (r = 0.813, p less than 0.01). Acute loss of atrial-ventricular pacing mode induced an increase in plasma ANP concentration from 44 +/- 8 to 104 +/- 13 pmol/l (n = 11, p less than 0.01) provided that systemic blood pressure was maintained. In contrast, if hypotension developed during ventricular pacing, the ANP levels fell from 68 +/- 11 to 14 +/- 7 pmol/l (n = 5, p less than 0.05) within five minutes despite elevation of atrial pressure. We therefore conclude that atrial pressure and the loss of atrioventricular synchrony may profoundly alter ANP release. The fall in plasma ANP concentration in acute hypotension suggests that, in addition to atrial pressure, ANP release is controlled by a peripheral negative feedback mechanism.

Aged↗
PubMed1986

Calcium antagonism--a new concept for treating essential hypertension.

Research on calcium antagonists has been prompted by the observation that the powerful vasodilatory effect of verapamil, as well as other calcium antagonists, is enhanced in hypertensive patients. Increased vascular resistance, seen in most types of hypertension, is determined by the intracellular free calcium concentration. The finding of an increased vascular responsiveness to calcium-channel blockade and the direct relation between the degree of antihypertensive response and the height of pretreatment blood pressure indicate abnormal intracellular calcium handling in patients with essential hypertension. This is supported by the observation that the intracellular free calcium concentration was significantly increased in patients with essential hypertension compared with normotensive subjects. The decrease in blood pressure with calcium antagonists was directly correlated with the patient's age and inversely with the pretreatment plasma renin activity. There was comparable antihypertensive efficacy among verapamil, nifedipine and nitrendipine. Increased understanding of pathophysiologic mechanisms in essential hypertension and pharmacotherapeutic studies have led to a new strategy for treatment of high blood pressure--in which calcium antagonists may be used, at least in part, as alternatives to diuretic drugs primarily in older and low renin patients with essential hypertension.

Age Factors↗
PubMed1986

Acute and chronic sympathetic reflex activation and antihypertensive response to nifedipine.

The importance of counterregulatory mechanisms triggered by arterial vasodilation for the antihypertensive response to the calcium entry blocking agent nifedipine was investigated in 13 men with mild to moderate essential hypertension. Blood pressure and systemic vascular resistance were significantly reduced 30 minutes after sublingual administration of 10 mg of nifedipine while heart rate, cardiac index and plasma norepinephrine concentrations increased (all p less than 0.01). Also, changes in mean blood pressure correlated inversely with arterial baroreflex sensitivity (r = -0.74, p less than 0.01), suggesting that arterial baroreflex mechanisms by means of sympathetic activation tend to limit the acute antihypertensive response. Blood pressure, but not systemic vascular resistance, decreased further (p less than 0.01) after 6 weeks of therapy with nifedipine 20 mg three times daily, while average heart rate, cardiac index and plasma norepinephrine concentrations had returned toward pretreatment values. Thus, a reduction of acutely increased sympathetic activity toward pretreatment values during long-term nifedipine therapy was associated with further decreases in blood pressure. The importance of sympathetic activity was also stressed by the finding of an inverse relation between chronic changes in heart rate and blood pressure (percent of control, r = -0.76, p less than 0.01). Blood volume did not change during long-term nifedipine therapy. The results suggest that the degree of sympathetic reflex activation in part determines the antihypertensive response to nifedipine monotherapy.

Adult↗
PubMed1986

Hemodynamic effects of nifedipine on hepatic venous pressure gradient in patients with portal hypertension.

The effect of Nifedipine on hepatic venous pressure gradient (HVPG) was determined in 10 patients with portal hypertension due to cirrhosis of the liver, and in 7 control subjects, by hepatic vein catheterization. Twenty min. after sublingual application of 10 mg Nifedipine, patients and controls showed significant hemodynamic changes in the systemic circulation. In contrast, HVPG after Nifedipine was not statistically different from the basal values--neither in patients with portal hypertension (p = 16.6 +/- 5.2 mmHg vs 17.9 +/- 5.3 mmHg) nor in the control subjects (p = 2.9 +/- 1.1 mmHg vs. 1.0 mmHg). We conclude that calcium entry blockade by Nifedipine is not effective in acutely reducing portal venous pressure.

Adult↗
PubMed1985

Age, race, blood pressure and renin: predictors for antihypertensive treatment with calcium antagonists.

Age, race, pretreatment blood pressure and plasma renin activity have been related to the antihypertensive response to calcium antagonists in studies that included 215 patients with mild to moderate essential hypertension. Adverse effects necessitated withdrawal from therapy in about 10% of the patients. All calcium antagonists lowered blood pressure significantly and comparably without weight gain or reflex tachycardia. In a multiple linear regression analysis of 138 white patients, age, pretreatment blood pressure and renin activity were of independent and significant predictive value for the antihypertensive response. Stratification of patients into 3 age groups disclosed a greater effect in patients older than 60 years compared with those between 40 and 60 years and those below 40 years, respectively (p less than 0.01). In 16 middle-aged black patients, antihypertensive therapy with a calcium antagonist proved highly efficacious. Monotherapy with a calcium antagonist may become a first-line treatment for essential hypertension, particularly in older patients who have low renin activity and possibly in black patients as well.

Adolescent↗
PubMed1985

Important differences between short- and long-term hemodynamic effects of amiodarone in patients with chronic ischemic heart disease at rest and during ischemia-induced left ventricular dysfunction.

To assess and compare the hemodynamic profile of short-and long-term amiodarone administration in the same set of patients and to investigate hemodynamic mechanisms responsible for the antianginal effect of this drug, 10 patients with documented coronary artery disease and stable angina pectoris were studied. Simultaneous right heart catheterization and equilibrium radionuclide angiocardiography were performed at rest and during exercise before therapy (control), after a 5 minute intravenous infusion of 7.5 mg/kg of amiodarone and after 21.0 +/- 4.3 days of peroral therapy (10 days 800 mg/day, 7 days 400 mg/day and then 200 mg/day). After acute drug administration, ejection fraction, stroke index and systolic blood pressure decreased, whereas heart rate, left and right ventricular filling pressures and systemic vascular resistance increased. These effects were reversed after long-term therapy; all measured values returned to control levels except for heart rate, which decreased below the control value, and right atrial pressure, which remained slightly elevated. Amiodarone drug levels decreased from 4.8 +/- 1.8 after intravenous infusion to 1.2 +/- 0.6 mg/liter after long-term therapy. After adjustment for hemodynamic changes at rest, there were still significant reductions in heart rate, mean arterial pressure and rate-pressure product during exercise. It is concluded that the marked negative inotropic effect of amiodarone administered acutely in the dose applied calls for cautious use of this drug when administered intravenously. In contrast, long-term oral amiodarone therapy seems hemodynamically safe, even in patients with moderately depressed left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗