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Biomedical subjects

T Meinertz

Publications and source records attributed to T Meinertz.

At least 253 records · Page 14Linked to original sources
PubMed1989

[Validation of a discontinuously recording, digital long-term ECG system (Siemens-Sirecust 802/850) using a single beat analysis].

Using beat-to-beat analysis we studied the annotation of 44 data-bases of the Massachusetts Institute of Technology (MIT) in comparison to the classification performed by a new microprocessor of a 24-h-ambulatory electrocardiographic device, which is based on real-time analysis and a solid-state ECG documentation. QRS detection was performed with an accuracy of 99%. Sensitivity and positive predictive accuracy were 70% and 87% for supraventricular ectopy. Using a fixed prematurity index of 80%, ventricular ectopy with a total of 7,845 beats was identified with a sensitivity of 64% and a positive predictive accuracy of 97%. With the additional consideration of late premature ventricular beats (PVB) sensitivity increased to 91% with a positive predictive accuracy of 96%. A sensitivity of more than 80% for singular PVB was achieved in 28/33 databases (85%), a similar positive accuracy was achieved in 27/33 databases (82%). Altogether, ventricular pairs and ventricular tachycardia resulted in a sensitivity of 83% and 76%, respectively, and in a positive predictive accuracy of 87% and 73%, respectively. Sensitivity exceeded 80% for ventricular pairs in 11/15 databases (77%) and for ventricular tachycardia in 10/14 databases (71%); similar results were observed for the positive predictive accuracy with 11/15 (73%) and 9/14 (64%) databases. In 42/44 databases and in all databases for arrhythmias of Lown class IVA and IVB, Lown classification was determined correctly. The Sirecust-Holter-ECG-system, a new device with real-time analysis and solid-state memory results in an accuracy for singular and complex ventricular arrhythmias, comparable to some of the presently available Holter systems.

Arrhythmias, Cardiac↗
PubMed1989

Electrophysiologic effects of enoximone in patients with congestive heart failure.

The electrophysiologic effects of enoximone were evaluated in 12 patients with idiopathic dilated cardiomyopathy undergoing routine programmed electrical stimulation (PES). Enoximone (1.5 mg/kg for 20 min followed by 0.75 mg/kg for 20 min) significantly shortened the spontaneous sinus cycle length as well as the atrial and ventricular refractory period. Neither during control PES nor during enoximone infusion were sustained ventricular arrhythmias provoked. However, in 5 of 12 patients, there was an increase in the number of repetitive ventricular responses induced by PES during enoximone administration. The observed electrophysiologic changes may be indicators for increased electrical instability of the myocardium in selected patients.

Adult↗
PubMed1989

Influence of enoximone on myocardial energetics in patients with idiopathic dilated cardiomyopathy: comparison with nitroprusside.

Enoximone may influence myocardial energetics by vasodilation, which may reduce and by inotropism which may increase myocardial energy demand. To separate both pharmacological properties, the influence of enoximone on myocardial oxygen consumption and its hemodynamic determinants was analyzed and compared to the effects of the pure vasodilator nitroprusside. The relationship between myocardial oxygen consumption and left ventricular hemodynamics was evaluated in 22 patients with idiopathic dilated cardiomyopathy (NYHA stages II-III). During control, myocardial oxygen consumption per beat [MVO2 (beat)] correlated closely with left ventricular systolic stress-time integral (STI) (r = 0.74; p less than 0.001). The ratio of MVO2 (beat) and STI was used as an inverse measure of the economy of myocardial contraction. Following nitroprusside (10 patients) the STI decreased by 35% (p less than 0.005) and MVO2 (beat) by 30% (p less than 0.005). MVO2 (beat)/STI did not significantly change. Following enoximone (12 patients), STI decreased by 60% (p less than 0.001), MVO2 (beat) by 19% (p less than 0.001), and MVO2 (beat)/STI increased from 1.31 +/- 0.16 to 2.72 +/- 0.78 nl.cm2/100 g.dyn.s (p less than 0.001). In summary, vasodilation by nitroprusside decreased MVO2 (beat) in proportion to its major determinant, STI; the economy of myocardial contraction remained unchanged. Compared to nitroprusside, enoximone reduced the economy of contraction. Thus, with enoximone, the energy-saving effect of vasodilation is counteracted by increased energy demand due to the inotropic stimulation of the myocardium. Global myocardial oxygen consumption depends on the balance of both pharmacological properties.

Cardiomyopathy, Dilated↗
PubMed1989

[Echocardiography detection of reversible regional disorders of contraction in patients with unstable angina pectoris and Prinzmetal angina during an attack].

We studied seven patients with Prinzmetal's angina and three patients with unstable angina pectoris type III (according to the criteria of Conti) during and after a spontaneous attack of angina pectoris by two-dimensional echocardiography. All patients underwent coronary angiography. The echocardiographic studies were performed during the attack (phase I), immediately after the attack (phase II), and 24 h after the attack (control). Left ventricular ejection fraction was significantly decreased during the attack (38.1 +/- 11% vs 59.8 +/- 7%), while left ventricular end-diastolic volume was increased (71.9 +/- 28 ml/m2 vs 50.3 +/- 13 ml/m2). The double product of heart rate and systolic blood pressure was equal at the 3 different examination times. In all patients transient regional disturbances of left ventricular contraction could be observed. In six patients the wall motion disturbances had already disappeared at phase II, while in four patients hypokinetic regions could still be found. At control, nine patients showed a normal left ventricular contraction pattern, while one patient with previous anterior myocardial infarction showed a small region of anterior akinesia. In all patients coronary artery obstructions were found in the same region of the left ventricle, where transient wall motion abnormalities occurred. Thus, two-dimensional echocardiography performed during an attack of angina pectoris in patients with Prinzmetal's angina and unstable angina pectoris type III can evaluate the localization, as well as the extent of transient myocardial wall motion abnormalities.

Angina Pectoris↗
PubMed1989

[Improved detection of acute myocardial infarct with combined simultaneous thallium-201/technetium-99m-PPi tomography in comparison with planar infarct scintigraphy].

UNLABELLED: The combined TI-201/Tc-99mPPi tomography was compared to planar Tc-99m-PPi scintigraphy in terms of diagnosis and localization of the infarction. In 32 consecutive patients with recent myocardial infarctions, the necrosis could be detected by means of planar imaging in 17 out of 22 patients with transmural and in three out of 10 patients with intramural infarctions. Six out of seven patients without recent myocardial infarctions were accurately diagnosed. Double radionuclide tomography made possible accurate diagnoses in all patients. Artefacts resulting from residual radioactivity within the cardiac blood pool and uptake of tracer in bones that overlie the heart were only observed with planar imaging. CONCLUSION: double radionuclide tomography is superior to planar imaging in the diagnosis of acute myocardial infarction.

Adult↗
PubMed1989

[Echocardiography in the diagnosis of lung embolism].

In the Federal Republic of Germany, approximately 10,000 to 20,000 persons die of pulmonary embolism (PE) each year. The mortality of treated PE is about 8% as compared with 18 to 35% in nondiagnosed PE. Massive PE is detected in only about 15 to 30% of the patients while, on the other hand, in 30 to 80% of those in whom PE is suspected the pulmonary angiogram may be normal. On use of pulmonary ventilation-perfusion scintigraphy, in 30 to 40% of the cases, both false negative as well as false positive findings have been described. ROLE OF ECHOCARDIOGRAPHY IN PATIENTS WITH ACUTE PULMONARY EMBOLISM. With echocardiographic imaging, the right heart as well as the central vessels in the proximity of the heart, in particular the pulmonary arteries, can be visualized. In addition to direct detection of right-sided-intraluminal thrombi, echocardiographic diagnosis is based predominantly on indirect signs, such as evidence of an acute cor pulmonale with dilatation of the right atrium and ventricle, the central pulmonary vessels and the inferior vena cava which, however, are relatively unspecific and may also be found in the presence of other diseases. Echocardiographic changes in acute pulmonary embolism can only be expected in the presence of increased pressure in the pulmonary circulation, that is, when at least a 30%-reduction in the cross-sectional area of the pulmonary vascular bed can be found. This can be documented in 60 to 70% of patients with acute PE. According to the literature and our own studies, of a total of 284 patients 84% had dilatation of the right ventricle, 70% paradoxic or hypokinetic motion of the interventricular septum in 102/141 patients there was dilatation of the right pulmonary artery. These changes regressed rapidly after therapeutic intervention. In about 30% of the patients a reduction in the left ventricular dimensions can be seen. Paradoxic septum motion and a decrease in the closing amplitude (EF-slope) of the anterior mitral leaflet can be seen. The extent of dilatation of the right ventricle and the right pulmonary artery correlate with the extent of the angiographic severity of acute PE provided that there is no marked preexisting left ventricular function impairment. NONINVASIVE ESTIMATION OF THE PRESSURE INCREASE IN THE PULMONARY CIRCULATION. On use of Doppler echocardiography, most patients with acute cor pulmonale have tricuspid regurgitation. This enables through determination of the systolic RV-RA pressure gradient an estimation of the systolic right ventricular pressure and, accordingly, the pulmonary artery pressure. In our experience, a systolic acceleration time in the pulmonary artery of less than 90 to 95 ms is

Echocardiography↗
PubMed1989

[Ventricular arrhythmia in silent myocardial ischemia--diagnosis and clinical relevance].

Silent myocardial ischemia and ventricular arrhythmias were known to be independent risk factors in patients with coronary artery disease. This has become more important since the technique of Holter monitoring has been improved and has demonstrated a high incidence of silent myocardial ischemia in the majority of patients with coronary artery disease, as well as a close relation to the occurrence of sudden cardiac death. Unfortunately, prospective data on the interaction of both risk factors are missing. We therefore studied patients undergoing exercise-testing, percutaneous transluminal angioplasty and 24-h-Holter-monitoring to assess such an interaction. During exercise testing the total incidence of ventricular arryhthmias in patients with asymptomatic ST segment depression was 42%; 6% of patients had frequent ventricular arrhythmias, 6% had ventricular pairs, and 1% had ventricular tachycardia. The incidence was similar to patients with symptomatic ST depression, but was 3.2-times higher as compared to patients without ST segment depression. During 103 attempts of percutaneous transluminal angioplasty, in 26 patients ventricular arrhythmias occurred, the incidence of ventricular tachycardia was 1-3%. No difference was observed for symptomatic and asymptomatic attempts. In 36 patients with severe coronary stenosis (greater than 90%) 24-h-Holter-monitoring showed 145 episodes of myocardial ischemia with a total duration of 967 min; two-thirds of episodes were asymptomatic. The incidence was similar in patients with symptomatic and asymptomatic episodes of myocardial ischemia, but 30 to 50-times higher as compared to the interval with ischemia. In summary, episodes of myocardial ischemia have a higher risk of ventricular arrhythmias, however, there is no difference between symptomatic and asymptomatic myocardial ischemia.

Arrhythmias, Cardiac↗
PubMed1988

Skeletal muscle blood flow, metabolism and morphology in chronic congestive heart failure and effects of short- and long-term angiotensin-converting enzyme inhibition.

Blood flow to skeletal muscle during exercise is limited in patients with chronic congestive heart failure compared with normal persons. This may, in part, be attributed to the inability of the vessels to dilate adequately. In addition, an abnormal skeletal muscle metabolism with oxidative capacity can be demonstrated in patients with chronic congestive heart failure. The latter may partially explain why vasodilators and inotropes that improve central hemodynamics, global leg perfusion or skeletal muscle blood flow during exercise do not increase oxygen uptake by working muscle after acute drug administration. Furthermore, increases in blood flow to skeletal muscle may be redistributed to inactive or less oxygen-dependent muscle fibers. Although acute angiotensin-converting enzyme inhibition usually neither exerts substantial improvement in exercise hemodynamics nor interferes with leg perfusion during exercise, skeletal muscle blood flow and oxygen uptake gradually increases with long-term angiotensin-converting enzyme therapy, leading to improved systemic oxygen consumption and exercise tolerance. Several factors, such as reduction in plasma and vascular angiotensin II and sympathetic nervous activity, increased prostaglandin levels and renal function may contribute to this beneficial long-term effect.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

The German multicenter trial of anisoylated plasminogen streptokinase activator complex versus heparin for acute myocardial infarction.

A multicenter randomized trial of anisoylated plasminogen streptokinase activator complex (APSAC) versus heparin in patients with acute myocardial infarction of less than 4 hours' duration was undertaken in 19 hospitals. Of the 313 patients, 151 received heparin and 162 APSAC (30 U as intravenous injection). Within 28 days of hospital stay, 19 deaths (12.6%) occurred in the heparin group and 9 deaths (5.6%) in the APSAC group (p = 0.032). After 24 hours, patients in the APSAC group had a significantly lower incidence of cardiogenic shock (3.2 vs 9.5%, p = 0.031), asystole (3.8 vs 10.8%, p = 0.015) and need for resuscitation (5.1 vs 11.5%, p = 0.039). There was no difference in global and infarct-related ejection fraction between the 2 groups. Thus, APSAC favorably influences prognosis and clinical course in hospital.

Anistreplase↗
PubMed1988

Mode of death in idiopathic dilated cardiomyopathy: a multivariate analysis of prognostic determinants.

A total of 110 patients with idiopathic dilated cardiomyopathy were followed prospectively for 53 +/- 8 (range 41 to 69) months to determine prognostic factors identifying patients at risk for sudden death or death from congestive heart failure. During the follow-up period 39 patients died, 14 of congestive heart failure and 25 suddenly. The incidence of cardiac death after 1 year was 18%, after 2 years 35%, and after 4 years 39%. Multivariate logistic regression analysis identified four independent prognostic factors: left ventricular ejection fraction, cardiac index, number of ventricular pairs/24 hours, and atrial rhythm (sinus rhythm or atrial fibrillation). With the final model of logistic regression 77 of 88 patients (88%) could be classified correctly as being at risk for death from chronic heart failure or sudden cardiac death. Patients who were likely to die of congestive heart failure were characterized by a markedly impaired left ventricular function (measured in terms of left ventricular ejection fraction, cardiac index, or both) and a low number of pairs/24 hours. The association between frequent complex ventricular arrhythmias and depressed left ventricular function identifies patients who are at risk for sudden death. The presence of atrial fibrillation significantly increases the risk of sudden death and death from congestive heart failure.

Adult↗
PubMed1988

Combination of calcium channel blocker and thrombolytic therapy in acute myocardial infarction.

To evaluate the protective effect of nifedipine on ischemic myocardium, in addition to thrombolytic therapy, a total of 149 patients with acute myocardial infarction were included in a double-blind controlled study in which they received 20 mg sublingual nifedipine (74 patients in group 1) or placebo (75 patients in group 2) in the emergency ward, either intracoronary nifedipine, 0.2 mg before and 0.2 mg after reperfusion of the infarct-related vessel and 20 mg three times/day during the hospital stay, or placebo. Combined intravenous and intracoronary thrombolytic therapy was initiated by means of mechanical recanalization in nonreperfused vessels. There were no differences between group 1 and 2 with regard to age, sex, body weight, or location of infarct. Evolution of CK-MB release and cumulative CK-MB was higher in group 1 than in group 2. Changes with regard to regional and global left ventricular function and coronary anatomy were not significantly different (NS) between the two groups. Reocclusion occurred in 15 of 74 (20%) and 10 of 75 (13%) patients in groups 1 and 2, respectively. During the reperfusion period, second- and third-degree atrioventricular block occurred in 5.4% and 6.7% (NS), ventricular couplets in 17.6% and 24% (NS), ventricular tachycardia in 2.7% and 9.3%, and ventricular fibrillation in 2.7% and 8% of the patients, respectively. Mortality rates were 13% and 8%. The study demonstrates that even very early administration of nifedipine combined with intracoronary administration does not enhance the salvage of ischemic myocardium achieved by reperfusion.

Adult↗
PubMed1988

Prediction of efficacy and tolerance of oral mexiletine by intravenous lidocaine application.

In a controlled crossover trial, 15 patients with frequent ventricular arrhythmias were treated with lidocaine to predict efficacy and safety of oral mexiletine. After an initial control period, patients received intravenous lidocaine (bolus infusion of 200 mg/20 min followed by 3.6 gm/24 hr and for 7 days oral mexiletine (200 mg four times a day). Efficacy was controlled by 24-hour Holter monitoring (responders = suppression of single premature ventricular beats [PVB] greater than 84% and of complex PVB greater than 90%). After lidocaine, 10 of 15 patients (67%) were responders (mean PVB reduction: 97%). After mexiletine, five of 15 patients (33%) were responders (mean PVB reduction: 81%); efficacy was closely related to the plasma concentration. When efficacy of both agents was compared, lidocaine infusion had a positive predictive value of only 50%; however, the negative predictive value was 100%. Thus in nonresponders to lidocaine, mexiletine is very likely to fail in the suppression of ventricular ectopy.

Administration, Oral↗
PubMed1988

[Diprafenone--comparative study of anti-arrhythmia therapy with propafenone].

Diprafenone is a new antiarrhythmic agent with a dominant local anesthetic action and additional beta-sympathicolytic activity. In a randomized study, we analyzed the antiarrhythmic efficacy and tolerance of diprafenone (450-600 mg/day) in comparison to that of propafenone (450-500 mg/day) in ten patients with frequent and complex ventricular premature beats. After an initial control period, all patients received either diprafenone 450 mg/day or propafenone 450 mg/day for 5 days. In the case of a drug response (VPB suppression greater than 84%, suppression of ventricular pairs greater than 90%, suppression of ventricular tachycardia greater than 100%), after a wash-out period of 7 days patients were treated with the second antiarrhythmic medication for 5 days. In the case of nonresponsiveness, the dose of diprafenone and propafenone was increased to 600 mg/day and treatment continued for a second 5-day period. During the control period and at every drug administration, 24-h-Holter monitoring and ECG were performed, and plasma concentration and side effects were checked. After individual dose titration, 7/10 cases were effectively treated with diprafenone (mean dose: 471 mg; mean VPB suppression: 92%) and 5/10 cases with propafenone (mean dose: 540 mg; mean VPB suppression: 80%). Altogether four patients reported side effects, mainly gastrointestinal, which limited therapy in one patient in each group. Compared to propafenone, diprafenone had a strong effect on AV-nodal and ventricular conduction intervals; however, in no patient was therapy limited by these changes. Thus, also in comparison to propafenone, diprafenone is effective in the treatment of ventricular arrhythmias.

Aged↗