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Biomedical subjects

S Klugmann

Publications and source records attributed to S Klugmann.

At least 55 records · Page 3Linked to original sources
PubMed1984

[Coronary spasm as a mechanism of ischemia or myocardial necrosis immediately after coronary surgery. Considerations on 5 cases and review of the literature].

Several recent reports suggest that coronary artery spasm may represent a major complication of coronary artery bypass surgery, and that it may have gone unrecognized in the past. During a three-year interval ending July 1983 we have encountered 5 cases in whom reversible S-T changes, angina, arterial hypotension, major arrythmias and/or angiography prompted the diagnosis of coronary arterial spasm early after aorto-coronary bypass surgery. Our experience and the review of 15 previously reported cases reveals that in most cases the clinical presentation was that of an acute, severe, ischemic cardiac event that occurred few hours after termination of cardiopulmonary bypass. A more benign course took place in a minority of cases, although some of them showed evidence of myocardial necrosis on ECG and/or left ventriculography. The mortality rate in the collective series was 20%, and the rate of perioperative non fatal myocardial infarction was 25%. Glyceryl trinitrate administration into the ascending aorta or into the spastic coronary artery appeared to be the most effective way of treating this condition, while the same drug was seemingly uneffective when administered intravenously. The use of calcium antagonists was associated with a favourable outcome in some patients, but on the whole the results were unpredictable. Prompt consideration of the possibility of coronary artery spasm and aggressive treatment are required in order to minimize its impact on perioperative mortality and morbidity rates.

Adult↗
PubMed1983

Effects of ICRF 159 on adriamycin-induced cardiomyopathy in rats.

The effect of ICRF 159 on adriamycin (ADR) cardiotoxicity and on total myocardial calcium content was examined in rats. ICRF 159 did not increase the survival time of ADR-treated animals; however the histological findings showed a significant prevention of ADR-induced cardiomyopathy (CMP) by ICRF. The total myocardial calcium content of animals treated with ADR was significantly higher, while no significant difference was seen in animals pretreated with ICRF 159 as compared with controls. As these findings suggested a role of calcium in ADR CMP and in the pharmacological action of ICRF in this disease, we also tested a closely related chelating agent, EDTA. This molecule decreased myocardial calcium levels in ADR-treated animals almost to normal values; however the histological cardiac alterations were not prevented.

Animals↗
PubMed1983

Acute hemodynamic effects of nifedipine at rest and during stress in severe aortic incompetence.

To determine whether afterload reduction with nifedipine is effective both at rest and during stress tests (rapid atrial pacing and contrast material overload), 14 patients with chronic severe isolated aortic insufficiency (10 asymptomatic) underwent right and left cardiac catheterization. Forty-five minutes after 20 mg of nifedipine (sublingually), left ventricular end-diastolic pressure, peak aortic pressure, systemic vascular resistance and double product decreased significantly at rest, at peak paced rate, and after angiography (P values from less than 0.05 to less than 0.001). Cardiac index increased at resting heart rate (P less than 0.01) but was unchanged during pacing. The reduction of systemic vascular resistances was inversely correlated with its initial value (r = -0.69). After nifedipine, average regurgitant fraction did not change; however its variations were significantly correlated with those of systemic vascular resistance (r = 0.69). It is concluded that in severe aortic insufficiency, nifedipine induces an effective reduction of left ventricular pre- and afterload, accompanied by an enhanced mechanical efficiency (unchanged or increased cardiac index with lower double product), both at rest and during stress tests.

Adult↗
PubMed1983

Calcium antagonists in heart failure.

Clinical experience with calcium antagonists in congestive heart failure has, to date, been mainly restricted to the use of nifedipine but there is either no or only a limited extent of information available on diltiazem and verapamil. In patients with acute and chronic congestive heart failure, single-dose administration of nifedipine was seen to lead to a decrease in systemic vascular resistance, left ventricular filling pressure and ventricular volumes as well as to an increase in stroke volume, ejection fraction and mean velocity of circumferential fiber shortening. These favorable effects could not be detected in eight patients during a three-week treatment phase with 80 mg nifedipine daily: resting blood pressure, cardiac volumes, echocardiographically-dimensions and exercise tolerance were unchanged as compared with placebo. In patients with ischemic heart disease and impaired ventricular function, in addition to an improvement in systolic function, single-dose nifedipine administration led to favorable effects on diastolic function with a shift of the diastolic pressure-volume relationship downward and to the diastolic pressure-volume relationship downward and to the left. In patients with severe aortic regurgitation, the observed increase in effective cardiac output affected by nifedipine was primarily attributable to an increase in heart rate. In the presence of an initially-elevated systemic vascular resistance, the regurgitation fraction decreased. In pulmonary hypertension, favorable hemodynamic effects have been reported after acute administration of verapamil as well as diltiazem and nifedipine. In individual cases, promising results in patients with primary pulmonary hypertension have been reported during long-term therapy with nifedipine provided that a favorable initial response could be documented.

Aortic Valve Insufficiency↗
PubMed1983

[Pharmacologic myocardial revascularization in acute infarct. Experience with 52 cases].

Coronary thrombosis is frequently demonstrated in the early hours of acute myocardial infarction. Local infusion of thrombolytic agents has been proposed in order to dissolve intracoronary thrombi and to restore myocardial perfusion. We report our initial experience in 52 patients. Thirty-nine males and 13 females had a coronary angiogram performed within 5 hours from the beginning of persistent ischemic pain (mean 2h 34 min +/- 68 min; range 20 min--5h 30 min). In all an ST segment elevation was documented on an ECG recording. Coronary occlusion was found in 86.5% (45/52) of our cases. Flow restoration was obtained in 39 of 45 of patients (86.6%) within 45 +/- 28 min. The mean dose of streptokinase employed was 272,140 +/- 112,484 IU (range 120,000--400,000 IU). Myocardial reperfusion was accompanied by the reduction of ischemic pain and ST elevation. In 8 cases severe ventricular arrhythmias occurred. Serious haemorrhagic complications were observed only in one patient. Eight patients developed a new myocardial infarction within few days from the procedure and two died 2 hours and 6 days respectively after myocardial revascularization. Thirty-two of thirty-nine patients underwent a angiographic control study within 11-128 days and coronary patency was shown in 75% (24/32). Seven patients underwent a coronary artery bypass procedure. At surgical inspection no clear evidence of myocardial necrosis was observed. Coronary flow restoration is rapidly and safely obtained i acute myocardial infarction by means of intracoronary streptokinase infusion but the efficacy of the procedure in salvaging myocardium has not been demonstrated yet.

Adult↗
PubMed1983

[Problems appearing after pharmacologic thrombolysis in acute myocardial infarct].

Pharmacologic myocardial reperfusion is a new strategy in the treatment of acute myocardial infarction, but its widespread use has raised several problems which are still unsolved. The time limit from the onset of ischemic pain until the beginning of thrombolysis is undefined yet. Experimental and clinical observations set this time within three hours. A reopened vessel is still at risk for reocclusion and anticoagulants are not always effective in the prevention of this. It is likely therefore that pharmacologic thrombolysis is only one step in the process of myocardial salvage and that other techniques like transluminal coronary angioplasty and/or coronary bypass surgery, should follow shortly. Intracoronary thrombolysis does not carry an increased risk for acute myocardial infarction patients. However haemorrhagic complications are expected to occur in less than 6% of cases during their hospital stay. To evaluate the extent of myocardial salvage quantitative ventriculography and intracoronary thallium 201 scintigraphy represent the most reliable techniques. Only the results of the continuing randomized trials will clarify the efficacy of this new way of therapy for morbidity, mortality and myocardial salvage.

Fibrinolytic Agents↗
PubMed1982

[Myocardial disease caused by adriamycin. Experimental animal models and possible pharmacologic prevention].

Adriamycin (ADR) is one of the most useful drugs in oncologic practice; it is effective not only against leukemias and lymphomas, but also against many solid tumors. A severe, frequent and dose dependent cardiomyopathy (CMP) limits its clinical use, therefore the cumulative dose usually administered is less than 550 mg/m2; however this procedure limits the therapeutic effectiveness of the drug. As this substance causes regression of a variety of neoplasms, during the past years a number of authors have studied the pathogenesis of the CMP. Data available on this subject are numerous but often in contrast. This review considers the experimental animal models used to study drug induced CMP; data on the biochemical mechanism underlying this complication and the efficacy of different antidotal procedures are also reviewed.

Animals↗
PubMed1982

Afterload reduction with nifedipine in aortic insufficiency.

The acute hemodynamic effects of nifedipine were assessed in 12 patients with severe aortic insufficiency during control conditions and 30 minutes after administration of nifedipine (20 mg sublingually). Left ventricular end-diastolic pressure decreased from 19 +/- 8 (mean +/- standard deviation) to 9 +/- 5 mm Hg (probability [p] less than 0.0001), mean aortic pressure from 98 +/- 12 to 80 +/- 9 mm Hg (p less than 0.00001), systemic vascular resistance from 1,135 +/- 280 to 794 +/- 176 dynes . s. cm-5 (p less than 0.0002) and rate-pressure product from 11,732 +/- 1,727 to 10,022 +/- 1,103 mm Hg beats/min (p less than 0.01). Forward cardiac index increased by 24 percent, from 3.8 +/- 1.1 to 4.4 to 0.8 liters/min per m2 (p less than 0.04). Left ventricular end-diastolic volume, ejection fraction and total stroke work index did not change significantly. Regurgitant fraction, measured in five patients, changed parallel with systemic vascular resistance. Left ventricular function was maintained while both preload and afterload were decreased. Regurgitant flow was moderated and myocardial oxygen demand decreased. This hemodynamically favorable condition, due to nifedipine, is clinically important and suggests the need for further therapeutic trials.

Adult↗
PubMed1982

[The transpulmonary distance in the evaluation of the pulmonary arterial pressure: roentgenographic-hemodynamic relations in mitral valve disease].

A linear correlation between transpulmonary distance and pulmonary arterial mean pressure was found in 84 patients with pure mitral valve disease. Neither the sum of the horizontal distance from the midline to the first divisions of the right and left pulmonary arteries, nor the measurement obtained dividing the transpulmonary distance by the maximum transverse diameter of the thorax significantly increase the correlation. DIP greater than 9.64 and 10.72 have 80% and 90% of chances of being associated with an abnormally high mean arterial pressure but correlate poorly with the extent of hypertension. Greater usefulness of the index might be obtained correlating it with the mean pressure measured under exercise.

Adolescent↗
PubMed1982

Hemodynamic effects of nifedipine in pulmonary hypertension.

Nifedipine is a calcium antagonistic drug which reduces elevated vascular resistances. The hemodynamic effects of 20 mg of sublingual nifedipine were studied in 10 patients with chronic pulmonary hypertension. The etiology of pulmonary hypertension was chronic lung disease in 4, congenital heart disease in 2, mitral stenosis in 1, recurrent pulmonary embolism in 2 and primary pulmonary hypertension in one case. 30' after the drug administration there was a fall both of total pulmonary vascular resistance (from 992 +/- 586 to 648 +/- 428 d s cm-5, p less than 0.02) and of systemic vascular resistance (from 1416 +/- 868 to 896 +/- 440 d s cm-5 p less than 0.02) with an increase of systemic cardiac index from 3.2 +/- 1 to 4.5 +/- 2 l/min/m'2 (p less than 0.02). No significant change in systemic arterial oxygen saturation was noted, while pulmonary arterial oxygen saturation increased from 56 +/- 16 to 62 +/- 13% (p less than 0.01). These hemodynamic changes persisted for 120' when a significant fall of mean pulmonary arterial pressure was also noted (from 59 +/- 11 to 52 +/- 9 mm Hg, p less than 0.02). These data indicate that nifedipine may be useful to reduce pulmonary resistance in pulmonary hypertension. However this effect was less pronounced in patients with chronic lung disease compared to the other cases. It is suggested that the type of pulmonary arterial changes may determine the hemodynamic response. Nifedipine may be particularly indicated when vasoconstriction (as in primary pulmonary hypertension) is the main determinant of pulmonary hypertension.

Adult↗
PubMed1981

[The retrograde catheterization of the aortic valve prosthesis. Usefulness and limits (author's transl)].

A retrograde catheterization of the left ventricle was performed in 10 patients with aortic valve prosthesis. The pulmonary wedge pressure increased during the procedure (median value 16 mmHg; range 1-33 mmHg). The sistolic aortic pressure (median value 26 mmHg; range 5-60 mmHg) and the diastolic aortic pressure (median value 16 mmHg; range 1-33 mmHg) decreased in all. In 5 patients a left ventriculography was performed. The left ventricle catheterization in patients with aortic valve prosthesis in the experience of the authors may preclude accurate hemodynamic measurements; it may be utilized only for the evaluation of an associated mitral valve disease.

Aortic Valve↗
PubMed1980

Primary pulmonary hypertension: effects of nifedipine.

The results of the medical treatment of primary pulmonary hypertension are usually very poor. A case of severe primary pulmonary hypertension in chronic heart failure was treated with the calcium antagonist nifedipine, a powerful vasodilator which acts directly on vascular smooth muscle. Nifedipine, administered in a dose of 20 mg sublingually, caused a pronounced fall in pulmonary and systemic vascular resistances (54 and 49%, respectively) and a rise in cardiac output (90.3%). Improvement was maintained over a three-month period. These data suggest that nifedipine can be used in the treatment of this condition.

Adult↗