[Non-invasive diagnosis of cardiomyopathies].
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Biomedical subjects
Publications and source records attributed to W Bleifeld.
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To assess the immediate haemodynamic and myocardial metabolic effects of the beta 1-agonist prenalterol, we studied by cardiac catheterisation the response to 50 and 100 micrograms/kg given intravenously in 16 patients with congestive heart failure secondary to coronary artery disease or non-ischaemic cardiomyopathy. At peak effect, cardiac index increased from 2.6 +/- 0.5 to 3.2 +/- 0.8 1/min/m2 (mean +/- SD) p less than 0.001); peak rate of left ventricular pressure development rose from 963 +/- 242 to 1355 +/- 411 mm Hg per second (p less than 0.001); left ventricular end-diastolic pressure fell from 27 +/- 6 to 13 +/- 7 mm Hg (p less than 0.001); coronary sinus blood flow increased from 120 +/- 39 to 147 +/- 55 ml/min (p less than 0.01); myocardial oxygen consumption was augmented from 12.9 +/- 3.9 to 15.7 +/- 5.8 ml/min (p less than 0.001); and heart rate increased slightly (76 +/- 12 to 86 +/- 14 beats per minute, p less than 0.05). No significant changes occurred in left ventricular systolic pressure, stroke volume index, myocardial lactate extraction rate, myocardial arteriovenous oxygen difference and no patient developed angina, ECG-changes or ventricular arrhythmias. Infusion of prenalterol effectively improved the haemodynamic function and cardiac metabolism in congestive cardiomyopathy.
1 The study was designed to elucidate further the mechanism by which beta-adrenoceptor antagonism with pindolol relieves the symptoms of angina pectoris in patients with coronary heart disease. 2 Pindolol administration was associated with an elevated threshold for angina pectoris and improved myocardial lactate metabolism during supraventricular pacing. 3 This beneficial effect of pindolol was independent of changes in myocardial blood flow and was not mediated by haemodynamic effects. 4 The results suggest that in angina pectoris, in addition to the recognized beneficial effects of beta-adrenoceptor blockade, the actions of pindolol also result from, as yet, poorly described phenomena such as redistribution of myocardial blood flow or metabolic effects.
In order to evaluate left ventricular function during dynamic exercise transoesophageal M-mode recordings of the left ventricle were carried out with a newly developed transducer gastroscope system. Twelve healthy subjects performed a graded supine bicycle exercise test. Stable and good quality images of the left ventricle at rest and during exercise at different steps up to a maximum workload of 100 watts were obtained in all patients. Isotonic maximum exercise resulted in a significant increase in fractional shortening of the left ventricle, peak shortening rate, and peak lengthening rate of the left ventricular minor axis. Left ventricular end-diastolic dimension decreased significantly. With increasing workload the pressure rate product increased significantly. It is concluded that transoesophageal M-mode echocardiography is a useful method of evaluating left ventricular performance during dynamic exercise.
Flashing tomosynthesis, a procedure that consists of a recording step and a reconstruction step, facilitates the tomographic imaging of coronary arteries. In a comparative study 10 postmortem coronary arteriograms were examined with 35-mm cine technique and with flashing tomosynthesis. The degrees of stenosis found with both of these techniques were compared with morphometrically obtained values. A higher correlation coefficient existed for the degrees of stenosis obtained with tomosynthesis and morphometry (r = 0.92, p less than 0.001, SEE = 9%) than for those obtained with cine technique and morphometry (r = 0.82, p less than 0.001, SEE = 16%). The technique has also been successfully carried out in 5 patients with coronary artery disease.
The value of transesophageal pulsed Doppler echocardiography (PDE) was studied in six patients with competent mitral valve and in 12 patients with angiographically proved mild to moderately severe mitral regurgitation. The results were compared with those from the standard transthoracic method of investigation. The advantages of the esophageal over the transthoracic approach in the detection of mitral regurgitation are (1) absence of anatomic obstacles between the ultrasound transducer and the heart; (2) nearly parallel alignment of the ultrasound beam with the blood flow direction; (3) the use of high pulse repetition frequencies; and (4) detection of localized regurgitant jets by left atrial scanning. This results in a superior recording quality and greater sensitivity. Based on a specific systolic flow pattern in the time-interval histogram, mitral regurgitation was detected in all patients by the transesophageal technique (100% sensitivity), but in only 58% by the precordial approach. Thus, transesophageal pulsed Doppler echocardiography can accurately detect the presence of mitral regurgitation, particularly in cases of mild or moderate severity.
Percutaneous transluminal coronary angioplasty (PTCA) was complicated by acute coronary artery occlusion associated with ST elevation and severe chest pain in three patients. Within 10 minutes, the occluded artery was reopened by an intracoronary (i.c.) infusion of streptokinase, resulting in the disappearance of chest pain and normalization of ST segments. To keep the artery patent, i.c. streptokinase had to be continued until emergency bypass surgery was performed. In two patients, no myocardial infarction occurred, as shown by a normal postoperative left ventricular angiogram. ECG and thallium-201 scintigram. In the other patient, who was admitted with an inferior infarction and underwent PTCA after i.c. lysis, no infarct extension was observed. These results show that i.c. streptokinase rapidly opens an acute coronary artery occlusion complicating PTCA, preventing myocardial infarction.
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Coronary sinus blood flow, great cardiac vein flow, myocardial oxygen consumption and myocardial lactate extraction were measured in 38 patients (12 female, 26 male) at rest and during supraventricular pacing until angina or av block occurred. 17 patients without significant coronary artery stenosis in the angiogram built the control group (group I). 15 patients had 2- or 3-vessel disease (group II), 6 exhibited an isolated LAD-stenosis of 80 to 95% cross section area (group III). There were no significant differences at rest between the 3 groups. Whereas pressure-heart rate product, coronary sinus blood flow and great cardiac vein flow, increased significantly during pacing in group I and II, there was only a slight increase in great cardiac vein flow from 77 +/- 22 to 83 +/- 19 ml/min in group III. Flow/beat only in this group declined significantly from 1.07 +/- 0.2 at rest to 0.68 +/- 0.1 ml during pacing (p less than 0.001). Coronary reserve capacity of these patients is probably reduced at rest, and flow during pacing can increase only insufficiently. Because rate-pressure product during pacing rose significantly, myocardial oxygen demand rose as well. The fact of a significant myocardial lactate production during pacing in group III indicates that increased myocardial oxygen demand in this group could not be adequately supplied. Also patients in group II produced lactate during pacing in contrast to patients of group I. So, if blood flow in the individual may be similar in patients with and without coronary artery disease, simultaneous measurements of myocardial lactate extraction can discriminate between both groups.
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