Biomedical subjects

M Pfisterer

Publications and source records attributed to M Pfisterer.

At least 73 records · Page 4Linked to original sources

PubMed1992

Effect of early intravenous heparin on coronary patency, infarct size, and bleeding complications after alteplase thrombolysis: results of a randomised double blind European Cooperative Study Group trial.

OBJECTIVE: To determine whether concomitant treatment with intravenous heparin affects coronary patency and outcome in patients treated with alteplase thrombolysis for acute myocardial infarction. DESIGN: Double blind randomised trial. TREATMENT REGIMENS: Alteplase 100 mg (not weight adjusted) plus aspirin (250 mg intravenously followed by 75-125 mg on alternate days) plus heparin (5000 units intravenously followed by 1000 units hourly without dose adjustment) was compared with alteplase plus aspirin plus placebo for heparin. SETTING: 19 cardiac centres in six European countries. SUBJECTS: 652 patients aged 21-70 years with clinical and electrocardiographic features of infarcting myocardium in whom thrombolytic therapy could be started within six hours of the onset of major symptoms. MAIN OUTCOME MEASURE: Angiographic coronary patency 48-120 hours after randomisation. RESULTS: Coronary patency (TIMI grades 2 or 3) was 83.4% in the heparin group and 74.7% in the group given placebo for heparin. The relative risk of an occluded vessel in the heparin treated group was 0.66 (95% confidence interval 0.47 to 0.93). Mortality was the same in both groups. There were non-significant trends towards a smaller enzymatic infarct size and a higher incidence of bleeding complications in the group treated with heparin. CONCLUSIONS: Concomitant intravenous heparin improves coronary patency in patients with alteplase. Whether this can be translated into improved clinical benefit needs to be to be tested in a larger trial.

Adult↗

PubMed1992

Clinical risk assessment after first myocardial infarction--is additional noninvasive testing necessary?

In order to assess whether the outcome of MI can be predicted by clinical data alone or whether and how much noninvasive testing is necessary to predict cardiac events or death, 361 patients were prospectively evaluated and followed for up to five years. A recursive partitioning analysis indicated that high-risk patients can be identified clinically after MI with a high degree of accuracy; to separate low-risk patients who need no further investigation or therapy, however, one additional noninvasive test is necessary which allows quantification of myocardial damage as well as exercise-induced ischemia. Additional tests added little to this risk prediction, indicating that multiple noninvasive testing should not be performed.

Adult↗

PubMed1991

[Are ECG criteria for indications for thrombolysis in acute myocardial infarct defined too narrowly?].

BACKGROUND: Despite the advantages of fibrinolytic therapy in acute myocardial infarction only about 20% of these patients receive this therapy. We studied patients excluded from fibrinolysis to identify subgroups with high mortality, which could derive benefit from more liberal interpretation of the indications for fibrinolytic therapy. METHODS: Retrospective chart review to identify patients with acute myocardial infarction in our coronary care unit 7/88-7/89. All patients received a questionnaire one year after this myocardial infarction. Patients not answering the questionnaire were contacted by phone or the information was sought from their physician. Indications for thrombolysis (with streptokinase or rTPA) were ST elevations of greater than or equal to 2 mm in greater than 2 adjacent leads and the absence of contraindications. RESULTS: In 231/242 (95%) of the identified patients a complete follow-up was obtained, 32% were age greater than 70 years, 30% were admitted greater than 6 h after the beginning of the symptoms, 64% did not fulfil the ECG criteria for thrombolysis, 21% (49/231) received thrombolytic therapy. The mortality after one year was 20.3% in patients not treated with thrombolysis and 8.2% in patients with thrombolysis (difference 12.1%, 95% confidence interval 2.9-21.3%, p = 0.048). Patients with preceding old infarctions (n = 58) fulfilled the ECG criteria for thrombolysis in a significantly smaller proportion (21% vs 41%, p = 0.004). Of all patients 12% were excluded from thrombolytic therapy due to a negative initial ECG and yet developed a Q ware infarction. The one year mortality of patients not given thrombolysis and with a Q wave infarction was 24% (22/93, p = 0.02 as compared to patients with thrombolysis), in patients with non Q wave infarction it was 13% (11/82, p = 0.41) and in patients with ambiguous ECG it was 57% (4/7, p = 0.006). The mortality in patients with a preceding infarction was 31% and significantly higher than in patients with a first infarction (16%, p = 0.049) and in patients receiving thrombolysis (8.2%, p = 0.005). CONCLUSIONS: By excluding patients with acute myocardial infarction from thrombolytic therapy a group with high first year mortality is selected. Most patients are excluded because of an initial ECG not showing enough ischemia to fulfil the criteria for thrombolytic therapy. A prospective study of thrombolytic therapy using less rigid ECG criteria in the subgroups with the highest mortality (patients with preceding myocardial infarction or ambiguous ECG) seems necessary.

Acute Disease↗

PubMed1991

Long-term treatment of ventricular tachycardia with amiodarone in presence of severe left ventricular dysfunction.

A group of 34 consecutive patients with coronary artery disease (n = 29) or dilated cardiomyopathy (n = 5) (3 women, 31 men, age 38-80 yr) who had severely impaired left ventricular function (left ventricular ejection fraction less than or equal to 40%) and high-grade ventricular ectopic activity (sustained or nonsustained ventricular tachycardia or ventricular fibrillation) were treated with amiodarone (mean dose: 206 mg/d) and followed for 1-117 (mean: 49) months. In the total group, there were seven sudden deaths, five deaths due to pump failure, one non-cardiac death, and two successful heart transplantations during follow-up. Thus the annual cardiac mortality in these carefully selected and followed patients was 8, 6%, the annual cardiac event rate was 10, 1%. The cumulative cardiac survival-rate was 62% after 5 years and 41% after 10 years. In five patients, treatment was interrupted after 10 to 43 months, three of the patients were alive at follow-up and two suffered cardiac death, resulting in an annual cardiac death rate of 12% in this subgroup of treatment. Based on the results of this retrospective analysis we conclude that in patients with low left ventricular ejection fraction and nonsustained or sustained ventricular tachycardia treated with low dose amiodarone, mortality was unexpectedly low. Thus, it may be the antiarrhythmic treatment to be considered in patients with ventricular tachycardia and severe left ventricular dysfunction.

Adult↗

PubMed1991

Coronary vasodilatation and improved myocardial lactate metabolism after angiotensin converting enzyme inhibition with cilazapril in patients with congestive heart failure.

The effects of angiotensin converting enzyme inhibition on systemic and coronary hemodynamics and on myocardial lactate metabolism were investigated before and 2 and 6 hours after cilazapril at rest and during supine submaximal exercise in 10 patients with New York Heart Association class II or III chronic congestive heart failure. Angiotensin converting enzyme inhibition, indicated by a significant increase in plasma renin activity, resulted in significant reductions in blood pressure and systemic vascular resistance. Myocardial oxygen demand decreased (resting double product 10.9 +/- 3.7 vs 12.2 +/- 3.8 mm Hg beats/min 10(-3); p less than 0.05), but coronary sinus blood flow remained unchanged and calculated coronary resistance decreased (0.45 vs 0.5 units, rest 6 hours; p less than 0.05) suggesting coronary vasodilatation. Changes in coronary vascular resistance were directly related to changes in systemic vascular resistance (r = 0.75, p less than 0.5). Myocardial lactate extraction increased at rest (47 +/- 60 vs 134 +/- 132 mumol/min; p less than 0.5) and during exercise (27 +/- 54 vs 491 +/- 317 mumol/min; p less than 0.05) both in patients with coronary artery disease (n = 5) and idiopathic dilated cardiomyopathy (n = 5). Resting lactate production was converted to lactate extraction in two patients with coronary artery disease. Neither plasma catecholamine nor atrial natriuretic peptide concentrations changed significantly. The results suggest coronary vasodilation and improved aerobic myocardial metabolism by angiotensin converting enzyme inhibition in patients with congestive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1991

Assessment of the extent of jeopardized myocardium during acute coronary artery occlusion followed by reperfusion in man using technetium-99m isonitrile imaging.

We tested the feasibility of technetium-99m methoxyisobutyl isonitrile (Tc-MIBI) imaging for delineating jeopardized myocardium during acute coronary occlusion and reperfusion in man. This new perfusion agent was injected in 25 patients during elective percutaneous transluminal coronary angioplasty (PTCA) of a single-vessel left anterior descending (LAD) coronary artery stenosis. Distinct perfusion defects were present on "occlusion" images but not on "open vessel" images obtained 20 to 24 hours later in 21 patients (84%). The extent and severity of perfusion defects were significantly smaller in patients with distal versus proximal LAD occlusions (3.4 +/- 1.2 versus 5.2 +/- 1.5 segments; p less than 0.001). The only factor that was significantly related to the presence or absence of such "ischemic" perfusion defects was the absence or presence of visible collateral vessels to the LAD (p less than 0.03). The site of occlusion, presence of wall motion abnormalities, or occlusion time did not influence the results significantly. Thus the myocardial area at risk could be visualized and quantitated by Tc-MIBI imaging even after occlusion times as short as 15 seconds, but functioning collateral vessels are capable of protecting jeopardized myocardium in this setting.

Adult↗

PubMed1991

Prolonged myocardial stunning after thrombolysis: can left ventricular function be assessed definitely at hospital discharge?

To assess whether myocardial dysfunction after acute reperfusion ('stunning') may show delayed recovery, 33 patients of the European Cooperative Study (rtPA vs placebo) had radionuclide angiocardiography on day 9 and after 3-6 months. Sixteen patients (13 inferior, three anterior infarcts) had a normal left ventricular ejection fraction (LVEF) which remained unchanged (55.4 vs 53.9%). In contrast, LVEF of 17 patients (10 inferior, seven anterior infarcts) with depressed values on day 9 improved during follow-up from 38.8 to 45.2% (P less than 0.01). Improvement was only observed in patients with early reperfusion defined a priori as peak creatine kinase value less than or equal to 15 h of pain onset (from 40.9 to 49.3%; P less than 0.05) in contrast to patients without reperfusion (from 34.0 to 35.2%; ns). Accordingly, LVEF increased in patients with open infarct-related arteries at hospital discharge (n = 8; P = 0.053) but not with persistent occlusion (n = 7; P = 0.11). Thus, a depressed LVEF observed 9 days after reperfusion may show delayed recovery due to prolonged stunning. Therefore, after thrombolysis, left ventricular function may not be evaluated definitively at hospital discharge; results of such studies should be interpreted with caution.

Adult↗

PubMed1991

Negative inotropic effects of antiarrhythmic drugs: a clinical point of view.

From a clinical point of view, the negative inotropic effects of antiarrhythmic drugs lead to the following questions: Do antiarrhythmic drugs induce or worsen congestive heart failure (CHF)? Which patients are at increased risk of developing CHF with antiarrhythmic drugs? Which antiarrhythmic drugs are most likely to induce CHF clinically? The present review of the recent literature demonstrates that antiarrhythmic drugs may induce or worsen CHF in a small number of patients. This is true for all antiarrhythmic drugs, but only disopyramide (and flecainide) are antiarrhythmic drugs with a relevant rate of clinical CHF. Patients with a history of heart failure, a low left ventricular ejection fraction, and cardiomyopathy are at increased risk of developing CHF with antiarrhythmic drugs, especially if the drugs are administered intravenously and in high doses.

Animals↗

PubMed1991

Effect of antiarrhythmic therapy on mortality after myocardial infarction.

In an attempt to improve survival of patients with coronary artery disease and high-grade ventricular ectopic activity, several studies using different antiarrhythmic drugs were undertaken. A meta-analysis of all randomized controlled trials using type I antiarrhythmic agents showed that the treatment effect was much more likely to be adverse than beneficial. In contrast to these studies, the pooled results of major secondary prevention trials using beta-blocking agents could demonstrate a significant reduction in the sudden death rate by an average of 24% during observation periods of 9-36 months. In the beta-blocker trials, however, patients with contraindications for this type of drug, such as overt congestive heart failure or chronic obstructive lung disease, were excluded. In these patients a type III antiarrhythmic drug, such as amiodarone, may have a place, and in fact, the Basel Antiarrhythmic Study of Infarct Survival, a prospective, controlled, randomized trial using low-dose amiodarone as an antiarrhythmic agent, could demonstrate a 60% reduction in sudden death rate and a 74% reduction in arrhythmic events incidence during the first year after myocardial infarction. Therefore, in patients with repetitive ventricular ectopic activity after myocardial infarction and adequate left ventricular function, a therapeutic attempt with beta-blockers without intrinsic sympathomimetic activity seems advisable. Beside beta-adrenergic blockade, low-dose amiodarone is an alternative, especially in patients with impaired left ventricular function or other contraindications for beta-blockers.

Anti-Arrhythmia Agents↗

PubMed1991

[Diagnostic procedures in patients with known coronary heart disease].

Patients with coronary artery disease can be stratified by noninvasive techniques into risk-groups for further diagnostic and therapeutic management. The prognostic impact of the patient's history, physical examination and ECG are discussed. With this clinical assessment a high-risk group of patients, who should undergo coronary angiography, can be identified. In a low-risk group, further evaluation depends on results of exercise-stress testing. The relative value of exercise ECG, thallium-201-scintigraphy and radionuclide ventriculography in this special clinical setting are discussed in detail.

Algorithms↗

PubMed1991

[Percutaneous transluminal coronary angioplasty].

Since its first application in a patient, PTCA has undergone a tremendous evolution: Based on growing experience and due to technical developments, indications have been markedly extended. Despite the fact that PTCA has been used in more risky situations, the primary success rate has risen and the rate of severe complications has dropped. This evolution is shown based on the Basel experience and on data from Switzerland. The problem of restenosis, however, has not been solved and remains the main problem to be looked for during follow-up of these patients.

Aged↗

PubMed1991

[Hemodynamic effects of a combination of general and peridural anesthesia during anesthesia induction in geriatric patients].

For major operative procedures in the lower abdomen and many orthopedic procedures such as total hip replacement, a combination of general and epidural anesthesia is used. In order to investigate the hemodynamic effects of such a combination in 14 geriatric patients aged 63-80 years who were undergoing total hip replacement, cardiovascular monitoring was established by an arterial line and a pulmonary artery catheter. The epidural anesthesia was achieved with bupivacaine 0.5% in a dose calculated to obtain a block up to Th 6. General anesthesia was then induced and maintained with midazolam, fentanyl, pancuronium bromide, and a 2:1 nitrous oxide-oxygen mixture. Hemodynamic measurements were established before and 30 min after induction of the epidural anesthesia and 20 min after the induction of general anesthesia. After bupivacaine was injected the loss of sympathetic tone produced a systolic arterial blood pressure decrease from 174 +/- 22 to 136 +/- 28 mmHg (p less than 0.05) and a decrease in heart rate from 73 +/- 12 to 66 +/- 10 min-1 (p less than 0.05). The cardiac index did not change, but the peripheral vascular resistance decreased significantly. Because intravenous fluids were given simultaneously, preload could be maintained. Oxygen delivery and oxygen extraction did not change. During general anesthesia a significant drop in cardiac output was observed from 3.0 +/- 0.6 l/min.m2 to 2.3 +/- 0.4 l/min.m2 (p less than 0.05). The systolic arterial blood pressure decreased to as low as 95 +/- 17 mmHg (p less than 0.05) and oxygen delivery decreased from 500 +/- 125 ml/min.m2 to 323 +/- 84 ml/min.m2 (p less than 0.05).

Aged↗

PubMed1991

Algorithm to predict triple-vessel/left main coronary artery disease in patients without myocardial infarction. An international cross validation.

Logistic regression was applied to the clinical, risk factor, and exercise data of consecutive angiographic referrals without prior myocardial infarction to determine an algorithm predicting the probability of triple-vessel/left main coronary artery disease. These data were obtained from a total of 1,074 such subjects from patient populations at four centers (Cleveland Clinic Foundation, Cleveland, Ohio; Hungarian Institute of Cardiology, Budapest, Hungary; the university hospitals, Zurich and Basel, Switzerland; and the Veterans Administration Medical Center, Long Beach, Calif.) and used to derive four separate probability algorithms. Each algorithm is based on patient data from study samples at three of the four centers and consists of 272 logistic functions, which are related to linear combinations of 13 variables (age, sex, type of chest pain, systolic blood pressure, resting electrocardiogram, serum cholesterol, fasting blood sugar, achieved exercise work load, achieved heart rate, exercise-induced angina and hypotension, heart rate-adjusted resting ST depression, and exercise ST slope). The four algorithms were cross validated by testing them on the populations not involved in their derivation. The resulting probabilities in the four test groups were then compared with the angiographic findings of triple-vessel/left main coronary artery disease. The discriminatory power of all the algorithms was fair to good (area under receiver operating characteristic curve, 0.68, 0.75, 0.82, 0.85) in the test groups. The algorithm did not significantly underestimate or overestimate disease probability except in one center (Long Beach).(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗

PubMed1990

[Coronary angiography, percutaneous transluminal coronary angioplasty and coronary surgery, valvular interventions and anti-arrhythmia agents and fibrinolysis for acute myocardial infarction in Switzerland].

Besides the description of the activities of the Working Group PTCA and Fibrinolysis of the Swiss Society of Cardiology, number and distribution of coronary angiograms and angioplasties (PTCA) and aortocoronary bypass operations performed in 13 Swiss centers during 1989 are presented and commented. It is of note that the number of PTCA procedures has increased further during the last year, whereas the number of bypass operations stayed fairly constant over the last three years. PTCA is done today almost as frequently as coronary artery bypass surgery in Switzerland. There are, however, marked differences between individual centers: the number of PTCA procedures in relation to coronary angiograms varies between 5% and over 40%. A large part of these interventions is performed at private hospitals. More than 85% of the PTCA procedures were single vessel procedures. Catheter interventions on heart valves and on the conductive system were done almost exclusively at University Hospitals. The 1989 survey of the treatment of acute myocardial infarction with fibrinolysis covers only hospitals with catheterization laboratories and is therefore not entirely representative for the total activity in Switzerland. Almost 20% (0-80%) of all patients admitted for acute myocardial infarction received fibrinolysis with important differences between individual centers.

Angiocardiography↗

PubMed1990

[Thrombocyte inhibitors in cardiovascular therapy].

An increased platelet-vessel wall interaction plays an important role in most forms of cardiovascular disease. In healthy arteries, the vascular endothelium prevents platelet adhesion and aggregation. As a mediator of this protective function, the endothelium produces prostacyclin, endothelium-derived nitric oxide and tissue plasminogen activator. Cardiovascular risk factors such as hypertension, hyperlipidemia and diabetes are associated with an increased platelet activation and with decreased antithrombotic properties of the blood vessel wall. The available inhibitors of platelet function interfere only with one of various mechanisms of platelet activation and of the platelet-vessel wall interaction. Prostaglandin inhibitors, such as aspirin and newer, more specific inhibitors, prevent the production and/or the effect of thromboxane A2 on platelets and the blood vessel wall. Other drugs interfere with the effect of adenosine diphosphate on platelets, or they increase intracellular concentration of cyclic GMP or AMP in platelets and vascular smooth muscle cells. The protective effects of platelet inhibitors in primary and particularly in secondary prevention of cardiovascular diseases have been documented in numerous studies. The successful clinical use of these substances, however, requires a selective prescription of the drugs in patients with cardiovascular disease.

Aging↗

PubMed1990

Direct vascular and myocardial effects of nisoldipine.

The effects of the dihydropyridine calcium antagonist nisoldipine on vascular smooth muscle and myocardium were investigated by brachial artery infusions and measurements of forearm blood flow and by intracoronary infusions and measurements of maximal rate of rise of left ventricular pressure (dP/dtmax). Brachial artery infusions (0.1 to 16 micrograms/min/1,000 ml tissue) in 10 patients with essential hypertension increased forearm blood flow and decreased calculated forearm vascular resistance dose dependently (maximal reduction of forearm vascular resistance 88%). A comparison with the vascular effects of verapamil indicated that the vasodilator potency of nisoldipine is approximately 40- to 50-fold greater in this model supporting similar results from in vitro experiments. Coronary artery infusions of nisoldipine (12, 24 and 48 micrograms over 3 minutes each) in 9 patients undergoing diagnostic left-sided cardiac catheterization did not change dP/dtmax. This lack of effect on left ventricular contractility was similar in patients with normal or impaired left ventricular function. Even though the coronary artery concentrations during the infusion are unknown, the highest intracoronary dose was comparable to the highest brachial artery infusion. Since the coronary vasculature has been found to be at least as sensitive to nisoldipine as the peripheral vasculature, it can be assumed that nisoldipine has no negative inotropic effect even in dosages that probably induced marked vasodilation. Thus, for nisoldipine and possibly other new dihydropyridine calcium antagonists, the concept of a dissociation between peripheral vasodilatation and direct myocardial effects also seems to apply to human circulation and the heart.

Adult↗

PubMed1990

[Clinical presentation and diagnosis of coronary heart disease].

Coronary artery disease may present as silent ischemia, chronic typical angina pectoris, unstable angina, Prinzmetal angina, acute myocardial infarction, and sudden cardiac death. These manifestations can usually be differentiated by the clinical history. Each of them has its own pathophysiology and, accordingly, therapy and prognosis are different. Myocardial ischemia is common to all of the manifestations and this can be assessed by history taking, ECG stress-testing, ambulatory monitoring, myocardial perfusion scanning, or radionuclide angiography (RNA). The diagnostic accuracy of these diagnostic procedures varies from 70% (history) to 81% (RNA).

Coronary Disease↗

PubMed1990

Prevention of aortocoronary vein bypass graft occlusion: which antithrombotic treatment and for how long?

The effects of 50 mg aspirin combined with 400 mg dipyridamole were compared with those of standard anticoagulant therapy, in the prevention of aortocoronary vein bypass graft occlusion. Early graft occlusion in 249 patients, with 749 distal vein graft anastomoses, were angiographically assessed 11.5 +/- 2 days after surgery and were almost equal in both treatment groups. In half of the patients in each group, active treatment was replaced by placebo after 3 months. Repeat angiography after 1 year (360 +/- 24 days) showed that more new late graft occlusions occurred in patients with only 3 months active medication (either regimen). The incidence of major complications was significantly higher in patients treated with anticoagulants, with minor side-effects more common in the antiplatelet group. Thus, this antiplatelet drug regimen was as effective as standard anticoagulant therapy in the prevention of early and late bypass graft occlusion, but carried a significantly lower risk of severe complications. In addition, as replacement of active treatment by placebo after 3 months resulted in significantly more graft occlusions, antithrombotic treatment should be continued for at least one year after coronary artery bypass graft surgery.

Adult↗