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Biomedical subjects

M L Simoons

Publications and source records attributed to M L Simoons.

At least 271 records · Page 15Linked to original sources
PubMed1985

Limitations of a QRS scoring system to assess left ventricular function and prognosis at hospital discharge after myocardial infarction.

The value of a QRS scoring system derived from 12 lead electrocardiograms to estimate left ventricular ejection fraction was assessed in a prospective study of 285 hospital survivors of myocardial infarction. In these patients both the QRS score and ejection fraction were measured by radionuclide ventriculography at discharge. The correlation between ejection fraction and QRS score was weak. In 22 patients who died during six to 12 months follow up the ability of the ejection fraction and QRS score to predict mortality was assessed in terms of sensitivity, specificity, predictive value of a positive and negative test, and efficiency. For ejection fraction less than 40% and a QRS score greater than or equal to 6 sensitivity was respectively 73% and 64%, specificity 73% and 56%, predictive value of a positive test 18% and 11%, predictive value of a negative test 97% and 95%, and efficiency 73% and 56%. Both ejection fraction and QRS score may be used to identify patients at low and high risk during one year follow up, but, contrary to initial expectations, the QRS score appears to be of little value in estimating ejection fraction and is less accurate than ejection fraction in predicting late survival in hospital survivors of myocardial infarction.

Adult↗
PubMed1985

Bleeding complications of intracoronary fibrinolytic therapy in acute myocardial infarction. Assessment of risk in a randomised trial.

The risk of bleeding associated with intracoronary infusion of streptokinase in acute myocardial infarction was determined in a randomised controlled trial containing 302 patients under the age of 70. Intracoronary streptokinase infusion was given to 152 patients and 150 patients were treated conventionally. Bleeding was seen in 24 (16%) patients in the streptokinase group and in two of the conventionally treated patients. Bleeding was most common (28%) in patients over the age of 60 years. The groin was the site of bleeding in all patients except one. In the first 48 hours after admission the haematocrit in streptokinase treated patients with manifest bleeding fell by 0.07 (0.04) (mean (SD)). The fall in haematocrit in the streptokinase treated patients without manifest bleeding was 0.05 (0.04) and in the conventionally treated patients it fell by 0.03 (0.04). Sixty six units of packed cells were transfused in the streptokinase group (50 units to those who bled); the control group required only 17 units. There were no deaths due to bleeding. The occurrence of bleeding and the fall in haematocrit in the streptokinase group correlated with the occurrence of systemic fibrinolysis but not with the dose of streptokinase given. Thus, in about 15% of patients treatment with intracoronary streptokinase resulted in significant non-fatal bleeding from the femoral puncture site that required substantial transfusion support. Furthermore, there was a significant drop in haematocrit in patients without manifest bleeding. These results emphasise the need for more specific fibrinolytic agents.

Clinical Trials as Topic↗
PubMed1985

Quantitative angiography of the left anterior descending coronary artery: correlations with pressure gradient and results of exercise thallium scintigraphy.

To evaluate, during cardiac catheterization, what constitutes a physiologically significant obstruction to blood flow in the human coronary system, computer-based quantitative analysis of coronary angiograms was performed on the angiograms of 31 patients with isolated disease of the proximal left anterior descending coronary artery. The angiographic severity of stenosis was compared with the transstenotic pressure gradient measured with the dilation catheter during angioplasty and with the results of exercise thallium scintigraphy. A curvilinear relationship was found between the pressure gradient across the stenosis (normalized for the mean aortic pressure) and the residual minimal area of obstruction (after subtracting the area of the angioplasty catheter). This relationship was best fitted by the equation: normalized mean pressure gradient = a + b . log [obstruction area], r = .74. The measurements of the percent area of stenosis (cutoff 80%) and of the transstenotic pressure gradient (cutoff 0.30) obtained at rest correctly predicted the occurrence of thallium perfusion defects induced by exercise in 83% of the patients.

Angiography↗
PubMed1985

Late results of reperfusion with intracoronary streptokinase.

Intracoronary streptokinase was infused to 152 randomly selected patients after acute myocardial infarction (MI). Control group consisted of 150 randomly selected patients after MI who were treated by conventional methods. Preliminary results indicate several beneficial effects of early reperfusion with intracoronary streptokinase.

Angioplasty, Balloon↗
PubMed1985

Effect of intracoronary thrombolytic therapy on global and regional left ventricular function. A three year experience with randomization.

The effect of myocardial reperfusion on regional left ventricular function has been quantitated by analysis of segmental wall motion in 185 patients enrolled in a randomized trial comparing thrombolysis with conventional treatment in patients with acute myocardial infarction. When analyzing the hemodynamic data on an "intention to treat" basis we found a significant preservation of left ventricular function after thrombolytic therapy when compared to conventional treatment. In addition, the wall motion analysis showed that a significant improvement of regional function in the "infarct zone" was observed in inferior infarction as well as in anterior infarction, although significant changes in regional function of the remote "non infarct zone" were observed at the acute as well as at the chronic stage. However, our follow-up data indicate that as yet it has not been resolved whether this method of treatment does indeed improve prognosis in patients with acute myocardial infarction. Accordingly, we maintain the view that such invasive treatment should not be generally applied until more follow-up data become available from larger randomized trials.

Aged↗
PubMed1984

Predischarge stress test after myocardial infarction in the old age: results and prognostic value.

The aim of this study was to evaluate the results of predischarge stress testing in the elderly, and to assess the prognostic value of the test during one-year follow-up. The database consisted of 48 patients older than 64 years of age and 109 patients 55-64 years of age, who survived acute myocardial infarction, out of 532 consecutive patients admitted for myocardial infarction. Stress-test results were not different in the two groups. During one-year follow-up mortality was 6% in the younger patients and 4% in the older group, and the incidence of non-fatal reinfarctions was 8% in both groups. Mortality was best predicted by the extent of blood pressure rise (43 +/- 26 mmHg in survivors vs 19 +/- 15 mmHg in non-survivors, P less than 0.001). Stress-test results were no more predictive when non-fatal reinfarction was added to mortality as an end-point. We conclude that for patients in whom the stress test is not contraindicated, age does not affect stress test results, the extent of blood pressure rise during a stress test is the best single predictor of mortality, stress tests are not predictive of reinfarctions.

Aged↗
PubMed1984

Clinical value of exercise testing in elderly patients.

Between 1978 and 1983, 1391 exercise tests were performed by 1083 males and 308 females over 64 years of age. This represents 17% of the total number of 8213 exercise tests. A history of myocardial infarction was present in 53% of the males and 30% of the females, while 12% of patients had previous heart surgery. Exercise was performed on a bicycle ergometer with stepwise workload increments of 10 or 20 W min-1. In 10% of patients the physician stopped the test because of serious arrhythmias or abnormal blood pressure response. The test was terminated because of fatigue (40%), angina (12%), dyspnea (18%) or tired legs and claudicatio (18%). Peak workload averaged 115 W in males and 85 W in females, which corresponds to 120% of the predicted normal values. Heart rate increased on average to 130 beats min-1 and systolic blood pressure increased to 180 mmHg. ECG changes compatible with myocardial ischaemia were observed in 42% of patients. Although elderly patients constitute a small fraction of the population referred for exercise testing, these findings indicate that the clinical value of the test when performed is similar to that in younger patients. The observation that most patients achieved higher than 'normal' maximum workloads may be due to unreliability of the reference values.

Aged↗
PubMed1984

Ineligibility for predischarge exercise testing after myocardial infarction in the elderly: implications for prognosis.

This study describes the clinical profile and prognosis of elderly patients not eligible for predischarge exercise testing. The database consisted of 133 patients 55-64 years of age, and 111 patients older than 64 years of age who survived an acute myocardial infarction. Follow-up was one year. In the younger age group, 24 (18%) patients were unable to perform the test, in contrast to 63 (57%) of the elderly subjects. In these two groups, one-year mortality rates were 13% and 37%, compared with 6% and 4% for the respective patients eligible for stress testing. Clinical profile and radionuclide ejection fraction between ineligible patients in both age groups were similar. Ejection fraction measurement was the best predictor of late mortality in those patients who did not have an exercise test. It is concluded that ineligibility for predischarge exercise test identifies a high-risk group, especially in patients older than 64 years of age.

Aged↗
PubMed1984

Haemodynamic effects of alinidine, a specific sinus node inhibition, in patients with unstable angina or myocardial infarction.

Alinidine is a new sinus node inhibitor which does not interact with the beta adrenergic receptors. Its haemodynamic effects were studied in 57 patients; 24 with unstable angina, 9 with myocardial infarction and heart rate greater than 100 bpm but without heart failure. 10 with myocardial infarction treated with vasodilators and 14 with severe heart failure or shock. After dosages up to 40 mg alinidine, heart rate decreased by 14 +/- 7 bpm, mean arterial pressure was reduced by 3 +/- 6 mmHg, stroke volume remained unchanged while cardiac output decreased 0.5 +/- 0.61 min-1 and systemic vascular resistance increased. Signs of heart failure developed in 3 patients, although overall left ventricular filling pressure remained unchanged. The haemodynamic response to alinidine warrants further studies of its efficacy in patients with angina or sinus tachycardia.

Adult↗
PubMed1984

Ventricular free wall rupture: sudden, subacute, slow, sealed and stabilized varieties.

Six cases of acute myocardial infarction with blood in the pericardial sac are described. In one case rapid death followed myocardial rupture leaving no time for the possibility of intervention. Of two other cases acute symptoms developing after myocardial rupture, one was operated on promptly and the other, whose condition improved on pericardiocentesis, after a delay of a few hours. Both are now long term survivors A fourth patient probably had two episodes of rupture which apparently sealed off. He underwent cardiac catheterization, but no epicardial leak was found. Subsequently at operation a sealed myocardial rupture was detected and sutured over. The fifth patient suffered a silent myocardial rupture. A false aneurysm was diagnosed four months later and he withstood successful surgery. In the sixth patient, the course was similar to that of case 1, namely rapid death with a clinical picture suggestive of tamponade. Postmortem examination showed a covert rupture with some evidence of attempts to plug the opening. The purpose of this report is to emphasize the varying course which myocardial rupture can take.

Acute Disease↗
PubMed1984

Prediction of mortality in hospital survivors of myocardial infarction. Comparison of predischarge exercise testing and radionuclide ventriculography at rest.

The relative merits of resting ejection fraction measured by radionuclide angiography and predischarge exercise stress testing were compared for predicting prognosis in hospital survivors of myocardial infarction. Two hundred and fourteen survivors of myocardial infarction out of 338 consecutive patients with acute myocardial infarction were studied over a 14 month period. Hospital mortality was 13% (45 of 338) whereas 19 additional patients out of 214 died in the subsequent year (9%). High, intermediate, and low risk groups could be identified by left ventricular ejection fraction measurement. Mortality was 33% for nine patients with an ejection fraction less than 20%, 19% for 58 patients with an ejection fraction between 20% and 39%, and 3% for 147 patients with an ejection fraction greater than 40%. Mortality was high (23%) in 47 patients who were unable to perform the stress test because of heart failure (19) or other limitations (28). The patients could be stratified further into intermediate and low risk groups according to the increase in systolic blood pressure during exercise: six deaths occurred in 46 patients with a blood pressure increase of less than 30 mm Hg and two deaths occurred in 121 patients with an increase greater than or equal to 30 mm Hg. Maximum workload, angina, ST changes, and ventricular arrhythmias were less predictive than blood pressure changes. It is concluded that the prognostic value of radionuclide angiography at rest and of symptom limited exercise testing is similar. The latter investigation should be the method of choice since it provides more specific information for patient management.

Aged↗
PubMed1984

Treatment of unstable angina with emphasis on calcium antagonists.

From the literature which has appeared over the last decade a selection was made of the three major calcium antagonists: nifedipine, verapamil and diltiazem. In the clinical situation, the net hemodynamic and electrophysiological effect of these drugs is the result of complex interactions between their peripheral and their central effects. The degree of baroceptor stimulation and reflex mediated beta-adrenergic activity, which counteracts and influences the intrinsic negative dromotopic, chronotopic and inotropic effects of calcium antagonists, are related to the degree of peripheral dilation. Nifedipine is the most potent arterial vasodilator and is consequently associated with the most intense reflex adrenergenic activity. Although their effects on vascular and cardiac muscle are similar but not identical, there exist major differences in their antiarrhythmic properties. All act as an antiarrhythmic agent when ischemia or reperfusion cause the arrhythmias, while verapamil selectively blocks the A-V node conduction. All three discussed calcium antagonists are effective in treating patients with coronary spasm, variant angina and unstable angina. In our personal experience with 73 patients with unstable angina with prolonged severe pain at rest with transient ST-segments and T-wavechanges without elevated enzyme levels, 21 became asymptomatic within 8 hours of treatment with conventional therapy, which included nitrates and betablockers. Of 52 who remained refractory to such therapy, the addition of 10 mg of nifedipine orally every two hours to a maximum of 60 mg rendered 42 of the 52 asymptomatic within 8 hours. Arguments why we believe that the timely administration of nifedipine to these and similar patients will reduce or delay the incidence of arrhythmias and myocardial infarction are given on the basis of experimental data. Nifedipine greatly dilates coronary arteries, an effect which persists even after the drug's general hemodynamic effects disappear. It is shown that antagonists have anti-ischemic properties which are primarily related to the persistent reduction of the basic coronary vascular tone which increases oxygen supply whilst reduced myocardial contractility leads to decreased oxygen consumption. Furthermore, preservation of cellular integrity is achieved via protection against intracellular Ca2+ excess, as demonstrated by preserved intracellular high energy phosphate. A randomized multicenter trial in the Netherlands is now in progress to clarify the definitive role of beta blockade versus calcium antagonists therapy of their combination in this syndrome.

Angina Pectoris↗
PubMed1983

Use of the fluid column in a cardiac catheter for emergency pacing.

Given the not infrequent need for intracardiac pacemaking during intensive cardiac care, a new type of cardiac pacemaker has been designed and tested [1]. With this pacemaker the heart can be stimulated through the fluid column of any conventional catheter, provided it is filled with a 0.9% NaCl solution. This fluid column pacemaker (FCP) is of the "constant current" type. The FCP was tested in 37 animals, in 30 patients in sinus rhythm, and also in two critical patients. In addition to the pacemaker circuit, a special connector was designed, enabling a fast, effective, and safe contact between patient and pacemaker. The FCP is considered to be ideally suited for use in emergency cardiac pacing in intensive care units and other areas where sudden bradycardias may occur and where intrathoracic catheters are inserted for a variety of reasons.

Animals↗
PubMed1983

Practical guidelines for treatment with beta-blockers and nitrates in patients with acute myocardial infarction.

Treatment of a patient with myocardial infarction might include opiates and sedatives to reduce pain and anxiety, heparin, antiarrhythmic drugs, diuretics which aim at improvement of myocardial function and drugs which might reduce the ischemic area at risk and thus mortality such as beta-blockers, vasodilators and possibly calcium antagonists. Obviously a selection of these and other therapeutic agents should be made for each individual patient. Guidelines for such a selection are presented in this paper. These are based on assessment of the hemodynamic state in a given patient: heart rate, blood pressure and presence or absence of heart failure as determined by non-invasive examination or by hemodynamic monitoring with a pulmonary artery catheter. An attempt should be made to reach an optimal hemodynamic state quickly, preferably within one hour of admission to the coronary care unit: a heart rate between 60 and 80 b.p.m., a systolic blood pressure between 100 and 140 mmHg and absence of signs of heart failure. For this purpose fast-acting intravenous drugs should be employed. Possibly myocardial preservation could also be achieved by prompt recanalization of an occluded coronary artery. At present, however, this is still an experimental procedure which should be further investigated.

Adrenergic beta-Antagonists↗
PubMed1983

Effects of captopril in acute and chronic heart failure. Correlations with plasma levels of noradrenaline, renin, and aldosterone.

The angiotensin-converting enzyme inhibitor, captopril, was given to 19 patients with severe heart failure. Seven patients had acute myocardial infarction and the remainder had chronic myocardial damage caused by ischaemia or valvular disease. Cardiac filling pressures were raised in all, the pulmonary capillary "wedge" pressure being 17 mmHg or more. Captopril, 50 mg orally, raised stroke volume and cardiac output, and reduced heart rate, cardiac filling pressures, systemic arterial pressure, and the plasma concentrations of aldosterone and noradrenaline. These changes were attended by clinical improvement. Decrements in cardiac filling pressures, systemic arterial pressure, and total peripheral resistance were positively correlated with pretreatment plasma renin. Long-term treatment with captopril was offered to 14 patients. Four patients with severe coronary disease died suddenly after initial clinical improvement. In nine patients haemodynamic measurements were repeated after three months. The results showed sustained effects on cardiac output and filling pressures but there was no loss of body weight. The haemodynamic effects were at least as good as with previous vasodilators. The fall in systemic arterial pressure, however, was greater with captopril. Captopril may become a valuable adjunct to the treatment of acute and chronic heart failure, but more information about its effect on coronary blood flow is required.

Aged↗
PubMed1983

What is preferable in unstable angina, beta-blockade or calcium-inhibition?

Nifedipine is a strong calcium antagonist; it blocks the excitation-contraction coupling, yet at therapeutic dosage levels it has few side effects. It is said that a single molecule of nifedipine can neutralize the effects of several thousand calcium ions in the excitation-process. Thus this agent reduces the ability of the cardiac cells to develop mechanical tension yet it does not affect electrical excitation. Calcium antagonists are also potent dilators, particularly of the arteries on the periphery of the human body and in the coronary arterial system. The basic mode of action is thought to be the same, i.e. reduction of the calcium transport, this time into the smooth muscle cells of the arterial wall, thus "forcing' the arteriole to dilate. The resultant action is a reduction in afterload, while there is an increase in perfusion of the coronary vascular bed. Thus there is a dual action, the one centrally, the other peripherally both of which will be particularly effective in patients with unstable angina (UA) in whom excess coronary vascular tone is suspected. Beta-blockers, particularly propranolol and metoprolol, with which we have the most experience, work via beta 2 adrenoceptor blockade in the heart. Cardiac frequency decreases, arrhythmias are suppressed, blood pressure may decrease, all reducing cardiac work. If in UA variations in coronary vascular tone and frank spasm do occur then is would be more logical to use Ca-antagonists instead of beta-blockade. Our clinical experience to date has not shown that patients with UA are worsened by propranolol or metoprolol but there are scores of clinical reports showing worsening of chest pain in Prinzmetal's syndrome, presumably because beta-blockade leads to excessive alpha-adrenergic vascular tone. On the other hand, in one year experience with 73 patients with UA, 52 did not experience relief from adequate beta-blockade until nifedipine was added. Within 2 hours, 42 of the 52 became asymptomatic--thus indicating that in UA the need for spasmolytic therapy prevails over the need for beta-blockade. In many cases of UA both drugs may have a place however, their exact relative value remains to be established.

Adrenergic beta-Antagonists↗