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Biomedical subjects

H Mehmel

Publications and source records attributed to H Mehmel.

At least 19 recordsLinked to original sources
PubMed1986

Asynchronous left ventricular wall motion early after coronary thrombosis.

To study regional wall motion early in the development of acute myocardial infarction, left ventriculograms performed in 24 patients before thrombolysis and within 3.5(1.2) (mean (SD] hours of the onset of pain were digitised frame by frame. Isometric and contour plots of regional wall motion were constructed. In 19 patients (seven with anterior descending, eight with right, and four with circumflex disease) thrombosis was demonstrated on an underlying stenosis. In 10 patients the two remaining coronary arteries were normal, and in nine, one or both showed important disease. Mean values of global indices of left ventricular function, including end diastolic volume, ejection fraction, peak ejection and filling rates, and cavity shape changes were all within normal limits, though end systolic volume was significantly raised. Total systolic amplitude of wall motion was normal in the affected area in all but seven patients (four with anterior descending, two with right, and one with circumflex thrombosis). Dyskinesis of more than 2 mm was seen in only three patients, all with thrombosis of the anterior anterior descending coronary artery, and hyperkinesis was present in four. The commonest abnormality of wall motion was hypokinesis during ejection followed by prolonged inward motion during isovolumic relaxation, which was seen in four patients with anterior descending, seven with right, and three with circumflex artery thrombosis. This was preceded by outward motion during isovolumic contraction and delayed inward motion during ejection in eight with right or circumflex thrombosis. Five of six patients without thrombosis had simple hypokinesis or dyskinesis without asynchrony. Disease of other coronary arteries did not affect the pattern of wall motion seen after right or circumflex coronary artery occlusion but it reduced the incidence of delayed inward motion along the free wall after thrombosis of anterior descending artery. Thus early after acute coronary thrombosis asynchronous wall motion is commoner than simple hypokinesis or dyskinesis. Its persistence suggests that in the setting of coronary artery thrombosis in man, residual contractile activity may persist for up to six hours after the onset of symptoms.

Acute Disease↗
PubMed1986

Changes in left ventricular regional asynchrony after intracoronary thrombolysis in patients with impending myocardial infarction.

Ventriculograms obtained before and a mean (SD) of 4.3 (2.5) weeks after intracoronary thrombolysis in 23 patients who were treated within 3.5 (3.1) hours of the onset of pain were examined for changes in asynchronous left ventricular wall motion. Lysis was achieved in 19 patients, and in 16 the affected artery was still patent at restudy. Angiograms were digitised frame by frame. Left ventricular volumes, ejection fraction, and peak ejection rate were all unchanged after thrombolysis, whereas peak filling rate fell, whether or not patency was achieved or maintained. Regional wall motion was examined by means of isometric and contour plots. The area supplied by the affected coronary artery showed simple hypokinesis or akinesis in 10 cases, which was unchanged at the second study in nine and improved in one. The commonest manifestation of asynchrony was delayed inward motion during isovolumic relaxation. This was present in 12 cases with or without associated hypokinesis; after thrombolysis wall motion improved significantly in eight and returned to normal in six, significantly more frequently than it did in patients with simple hypokinesis. Dyskinesis (three patients) and hyperkinesis (five patients) resolved in all. Outward wall motion during isovolumic relaxation reverted to normal in four out of five cases, and outward motion during isovolumic contraction reverted to normal in five out of seven. The frequency of improvement was also increased when the circulation to the affected segment was not compromised by an important residual stenosis. Flow in the affected artery was re-established or maintained significantly less frequently when simple hypokinesis or akinesis was present at the first study. These observations provide further evidence that asynchronous wall motion early after acute myocardial infarction represents residual contractile activity, and suggest that knowledge of its presence and distribution may be useful in assessing patients on whom thrombolysis is performed.

Coronary Angiography↗
PubMed1984

Effect of successful thrombolytic therapy on right ventricular function in acute inferior wall myocardial infarction.

In 19 patients undergoing intracoronary fibrinolytic therapy for acute myocardial infarction, the site of coronary obstruction was in the proximal right coronary artery. Time between onset of symptoms and hospitalization was less than 4 hours. These patients were studied prospectively by radionuclide techniques immediately after admission, 48 hours and 4 weeks after AMI. Right and left ventricular (RV and LV) ejection fractions (EF) were calculated from gated blood pool scintigrams and the size of the LV perfusion defect was assessed by thallium-201 scintigraphy. Before the intervention, RV performance was significantly lower (RVEF 29 +/- 8%) than normal (53 +/- 7%). The size of the LV perfusion defect was relatively small (less than 25% of LV circumference), and as a consequence, LV pump function was only marginally impaired (LVEF 54 +/- 11%). Recanalization of the infarct artery was achieved in 12 patients (group A); in 7 patients the infarct artery remained occluded (group B). Early after the intervention (48 hours), RV performance in group A recovered significantly (RVEF: 30 +/- 9% vs 39 +/- 7%, p less than 0.01), and further improvement was noted at 4 weeks (RVEF 43 +/- 5%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Noninvasive assessment of myocardial contractility in asymptomatic patients with sever aortic regurgitation and normal left ventricular ejection fraction at rest.

In 14 asymptomatic patients with isolated aortic insufficiency the slope k of the end-systolic pressure-volume relation was determined noninvasively with equilibrium radionuclide angiography. The results were compared with changes in left ventricular ejection fraction during maximal physical stress. Nine normal volunteers served as a control group. Patients with aortic insufficiency did not differ significantly from the control group with respect to left ventricular ejection fraction at rest (aortic insufficiency 62 + 8 percent, control 65 +/- 6; probability [p] = not significant [NS]), physical work capacity (aortic insufficiency 113 +/- 32 watts, control 117 +/- 25; p = NS) or age (aortic insufficiency 40 +/- 10 years, control 47 +/- 7; p = NS). The slope (k) of the end-systolic pressure-volume relation was found to be significantly lower in the group with aortic insufficiency (3.1 +/- 1.1) than in the control group (4.1 +/- 0.5; p less than 0.05). Patients with aortic insufficiency could be classified into two subgroups with respect to the slope k. In subgroup A (n = 7) the slope fell within the normal range (4.0 +/- 0.6) as defined by the control group, and the left ventricular exercise reserve was normal (6 percent +/- 1). In subgroup B (n = 7) the slope was significantly lower (2.2 +/- 0.6, p less than 0.01), indicating depressed myocardial contractility, and all patients experienced left ventricular dysfunction during exercise (left ventricular exercise reserve -5 +/- 5 percent). Thus, noninvasive determination of the end-systolic pressure-volume relation identified two subsets of asymptomatic patients with aortic insufficiency, one with impaired myocardial contractility and normal left ventricular exercise reserve and a second group with depressed myocardial contractility and left ventricular dysfunction during exercise. Therefore, an abnormal baseline contractile state in asymptomatic patients with aortic insufficiency may be uncovered by noninvasive determination of the end-systolic pressure-volume relation or by assessing the left ventricular exercise reserve. Serial studies in a larger group of patients undergoing surgical correction of the valve lesion are indicated to determine whether this information will be helpful in evaluating when to operate on asymptomatic patients with aortic insufficiency.

Adult↗
PubMed1982

Thrombolysis in acute myocardial infarction using intracoronary streptokinase: assessment by thallium-201 scintigraphy.

Twenty-one patients with acute myocardial infarction, admitted to the hospital within 4 hours after the onset of symptoms, were studied by seven-pinhole thallium-201 scintigraphy before and 1 hour and 24 hours after intracoronary fibrinolysis using streptokinase. The size of the thallium-201 perfusion defect was assessed from myocardial cross sections reconstructed from the original seven-pinhole data and expressed as a fraction of left ventricular circumference. Recanalization was achieved in 16 patients within 3.9 +/- 1.6 hours after onset of symptoms (group A). In these patients, the size of the perfusion defect had decreased from 36 +/- 17% to 19% +/- 15% (p less than 0.001) at 24 hours. No significant change was detected by redistribution at 1 hour after the intervention. In five patients, intracoronary fibrinolysis was unsuccessful, and the vessel remained occluded (group B). The thallium-201 perfusion defect affected 40 +/- 15% of the left ventricular circumference before the intervention; it remained virtually unchanged at 1 hour (37 +/- 16%) and at 24 hours (41 +/- 15%) after fibrinolysis. The perfusion defect was most reduced in patients with extensive collaterals supplying the ischemic area or with subtotal occlusion of the affected coronary artery. We conclude that successful intracoronary fibrinolysis may reduce the size of the thallium-201 perfusion defect in many patients with acute myocardial infarction. One important factor in the final result may be the presence of residual coronary flow supplied by extensive collaterals or by subtotal occlusion of the affected coronary artery when reperfusion is achieved around 4 hours after the onset of symptoms.

Adult↗
PubMed1981

[The effect of tricuspid insufficiency on right ventricular performance in patients with valvular heart disease (author's transl)].

The hemodynamic effect of tricuspid insufficiency on right ventricular function was studied in 25 patients with rheumatic heart valve disease. 10 patients had mixed valve disease without tricuspid insufficiency (group A), and 15 patients had mixed mitral valve disease with tricuspid insufficiency (group B). Mitral valve area (1.76 vs. 1.66 cm2) and mitral regurgitant fraction (55 vs. 45%) were not significantly (p greater than 0.05) different between groups. Patients of group B revealed higher right atrial and right ventricular end-diastolic pressures than patients of group A. Right ventricular ejection fraction was lower in group B as compared to group A (44 vs. 52%, p less than 0.05). During ergometric exercise right atrial pressure was higher in group B as compared to group A (19 vs. 14 mm Hg, p less than 0.05), but mean pulmonary artery pressure (48 vs. 51 mm Hg, p greater than 0.05), cardiac index (3.3 vs. 3.31/min . mi2, p greater than 0.05) and stroke index (27 vs. 25 ml/m2, p greater than 0.05) were not significantly different. In mixed mitral valve disease associated with tricuspid regurgitation, right ventricular function is impaired when compared to mixed mitral valve disease of equal severity but without tricuspid regurgitation. Exercise induces a further augmentation of right atrial pressure in these patients with tricuspid regurgitation. We conclude, right atrial pressure elevation is not only the consequence of tricuspid regurgitation in group B but also the consequence of impaired right ventricular function. Impairment of right ventricular function is further augmented during exercise.

Adult↗
PubMed1976

[Congestive cardiomyopathy (author's transl)].

Congestive cardiomyopathy principally affects adolescent young men. The prognosis is very serious, mortality is almost 50%. Symptomatology, clinical and radiological findings are chiefly determined by signs of cardiac insufficiency. The ECG almost always shows a pathological but not a pathognomonic finding. If ventricular dilation is marked, left ventricular function is partly extremely limited. As causes of congestive cardiomyopathy, inflammatory changes, autoimmunological processes and metabolic disorders are discussed.

Adult↗