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Biomedical subjects

H Just

Publications and source records attributed to H Just.

At least 307 records · Page 17Linked to original sources
PubMed1987

[Relation between hemodynamics and ventricular arrhythmia in patients with heart valve diseases].

The incidence and severity of ventricular arrhythmias were compared with hemodynamic findings of cardiac catheterization, in 160 patients with mitral and aortic valve disease. All patients underwent right and left heart catheterization, as well as M-mode and 2D-echocardiography, and 24-hour ambulatory electrocardiographic monitoring. Out of 160 patients, 68 had mitral valve disease and 92 had aortic valve disease. In mitral regurgitation the degree and frequency of ventricular arrhythmias showed a positive correlation to the degree of regurgitation (rs = 0.44, rs = 0.56, respectively) and a negative correlation to left ventricular ejection fraction (rs = -0.49, rs = -0.57) and to cardiac index (rs = 0.48, rs = 0.53). In aortic valve disease the incidence and severity of ventricular arrhythmias were not related to the type of valve lesion, to the transvalvular pressure gradient nor to the degree of regurgitation. In aortic stenosis, the degree of arrhythmia showed a negative correlation to left ventricular ejection fraction (rs = 0.55) and a positive correlation to left ventricular endsystolic volume index (rs = 0.40) and to peak systolic left ventricular wall stress (rs = 0.59). In aortic regurgitation the number of ventricular arrhythmias showed a negative correlation to left ventricular ejection fraction (rs = -0.43) and a positive correlation to left ventricular endsystolic volume index (rs = 0.43) and to peak systolic left ventricular wall stress (rs = 0.37). These data demonstrate that the incidence and severity of ventricular arrhythmias, in patients with aortic valve disease and mitral regurgitation, are strongly associated with the impairment of left ventricular function.

Adult↗
PubMed1986

[Calcium antagonists in heart failure?].

Although beneficial acute hemodynamic effects of calcium antagonists in heart failure have been reported, their use in this setting is still controversial because of the negative inotropic effects produced by these agents. The direct actions of calcium antagonists, that is direct depression of myocardial contractility and coronary and peripheral vasodilation, are modulated by systemic hypotension-induced baroreceptor activation of autonomic reflexes. Thus, at clinically relevant dosages, the baroreceptor-mediated cardiac stimulatory effects may counterbalance or override the direct negative-inotropic effects, as usually observed with nifedipine or diltiazem. By contrast, with verapamil significant depression of contractility may occur. Newer calcium antagonists with higher vasoselectivity such as nisoldipine or felodipine may be particularly interesting in the setting of congestive heart failure because of pronounced arterial vasodilatation and their additional effects on coronary blood flow, LV-regional wall motion and diastolic function and peripheral blood flow distribution with negligible myocardial effects. Due to their marked vasodilatating properties, newer derivatives may be advantageous in the treatment of heart failure due to coronary artery disease and hypertension. Although limited data concerning long-term efficacy are available, preliminary studies suggest long-term benefit in selected patients. It appears that verapamil should not be used for vasodilator therapy of severe heart failure, since deterioration of LV function may occur.

Calcium Channel Blockers↗
PubMed1986

Coronary thrombolysis during acute myocardial infarction by intravenous BRL 26921, a new anisoylated plasminogen-streptokinase activator complex.

The safety and fibrinolytic efficacy of a new anisoylated plasminogen-streptokinase activator complex (APSAC) was tested in 50 patients with acute myocardial infarction (AMI) less than 4 hours in duration. APSAC (30 mg) was given intravenously as a bolus injection 151 +/- 47 minutes after clinical symptoms. Coronary angiography was then performed to assess coronary artery patency: 28 patients had an inferior AMI and 22 an anterior AMI. A patent infarct-related artery was found in 32 patients (64%) on first coronary angiography 66 +/- 21 minutes after administration of APSAC. Subsequent reperfusion was observed in 10 patients after 74 +/- 16 minutes (84%). Bleeding complications or hematomas were observed in 18 patients, of whom 3 required blood transfusions. Marked hypofibrinogenemia was observed within 24 hours in most patients. A control coronary angiogram was recorded in 37 patients (74%) after 25 +/- 19 days and showed reocclusion in 5 patients.

Adult↗
PubMed1986

Intravenous fibrinolytic therapy of acute myocardial infarction: new perspectives from plasminogen activators?

The early treatment of acute myocardial infarction has changed rapidly in recent years. Given the fact that an occlusive coronary thrombus can be found in most infarct patients within 4 h after clinical symptoms, the idea of instituting medical or mechanical recanalization of the occluded vessel is intriguing. However, invasive measures are time consuming, expensive and not freely available to a great number of patients. Thus, only i.v. fibrinolytic therapy of acute myocardial infarction will gain wider application in the near future. Several concepts have been worked out, one of which uses a high-dosage streptokinase or urokinase regimen. A different therapeutic alternative has been made possible by the development of selective fibrinolytic substances, such as the tissue-type plasminogen activator (t-PA) or the anisoylated plasminogen-streptokinase activator complex (APSAC). Preliminary clinical data have shown that the coronary artery patency rate achieved after i.v. administration of t-PA or APSAC is higher than that after conventional treatment with streptokinase or urokinase. The incidence of severe bleeding complications is low and comparable in these studies. However, until myocardial salvage has been demonstrated with early i.v. fibrinolytic therapy in acute myocardial infarction in a placebo-controlled randomized trial, this therapeutic concept will still be unsettled.

Anistreplase↗
PubMed1986

Assessment of myocardial function by calculation of two energetic parameters from pressure-volume relations and wall thickness in human ventricles.

For defining myocardial performance in chronic cardiac diseases and during acute pharmacological interventions we created a new index of performance based on myocardial mechanical and energetic counterparts. From angiocardiographic pressure-volume data the pressure-volume integral is analyzed and divided by left ventricular muscle mass, yielding work done by a unit of myocardium (E1). From pressure-volume data the stress-time integral integral of sigma.t is evaluated by using an ellipsoidal calculation model. In order to compare E1 with the integral of sigma.t the integral of sigma.t is transformed into energetic units on the basis of new physiologic myothermal findings (E2). Then, the sum of E1 and E2 (i.e.,the maximum of mechanical performance), the ratio of E1 to the sum of E1 and E2 can be defined (i.e., the myocardial work related to the energy consumed during a contraction). By calculating E1 and E2, we are able to analyze the myocardial efficiency of work production. These parameters are proposed for judging the myocardial performance and efficiency in congestive heart failure and the effects of positive inotropic substances and vasodilators.

Angiocardiography↗
PubMed1986

Myothermal economy of rat myocardium, chronic adaptation versus acute inotropism.

By means of rapid planar Hill type antimony-bismuth thermophiles the initial heat liberated by papillary muscles was measured synchronously with developed tension for control (C), pressure-overload (GOP), and hypothyrotic (PTU) rat myocardium (chronic experiments) and after application of 10(-6) M isoproterenol or 200 10(-6) M UDCG-115. Economy of force production was analyzed by the ratio of initial heat versus developed tension-time integral. This ratio was found to be reduced by 34% in GOP and by 43% in PTU myocardium (P less than 0.01, respectively) indicating increased economy of force production. In contrast, isoproterenol increased initial heat versus tension-time integral by 70% (P less than 0.01) indicating reduced economy of force production. No change in this ratio was found for UDCG-115. The presented data indicates that long and short term modulation of myocardial energetic costs of force generation is possible. The basic mechanisms for these myocardial alterations are discussed.

Animals↗
PubMed1986

Noninvasive evaluation of pulmonary hypertension by quantitative contrast M-mode echocardiography.

Although it has been shown that pulmonary flow velocity can be calculated from contrast M-mode echocardiographic tracings, the clinical value of this noninvasive method has not been established. We used contrast M-mode echocardiography to examine the flow velocity pattern at the pulmonary valve in 30 adults referred for diagnostic cardiac catheterization. In the 15 patients with normal pulmonary artery pressure (PAP) (mean pressure less than or equal to 20 mm Hg), midsystolic pulmonary flow velocity was significantly (p less than 0.001) higher (654 +/- 140 mm/sec) compared to the 15 patients with pulmonary hypertension (342 +/- 85 mm/sec, mean pressure greater than 20 mm Hg). Fourteen of the 15 patients with pulmonary hypertension exhibited an early systolic flow velocity peak, whereas all patients with normal PAP showed a dome-shaped systolic flow velocity profile with maximal flow velocity occurring in midsystole. A significant close correlation was found between the relative early to midsystolic flow velocity change and mean PAP (r = 0.96; p less than 0.001). Thus quantitative contrast M-mode echocardiography reliably differentiates patients with pulmonary hypertension from patients with normal mean PAP. In addition, this technique allows a noninvasive estimation of PAP.

Adolescent↗
PubMed1986

Echocardiographic findings in patients with proved pulmonary embolism.

Echocardiographic studies were performed in 105 patients with acute and recurrent pulmonary emboli. Pulmonary embolism was confirmed by pulmonary angiography (n = 48), autopsy (n = 6), and lung perfusion scintigraphy (n = 51). Seventy of 93 patients (75%) displayed a dilated right ventricle, 38 of 91 patients (42%) had reduced left ventricular cavity dimension, 41 of 82 patients (50%) had a decreased EF slope of the mitral valve, and 78 of 101 patients (77%) showed dilatation of the right pulmonary artery. The motion of the interventricular septum was abnormal in 41 of 93 patients (44%). Right-sided thrombi were seen in 13 patients within the right pulmonary artery (n = 11) and in the right ventricle (n = 3); in one patient they were found in the superior vena cava, in the innominate vein, and the right atrium. Two patients suffered from right-sided endocarditis. Thus echocardiographic changes were frequently found in patients with proved pulmonary emboli. The echocardiographic findings of right-sided cardiac and pulmonary artery abnormalities indicate hemodynamically active pulmonary emboli.

Acute Disease↗
PubMed1986

Quantitative assessment of temporal and spatial ventricular wall motion in normal and infarcted human left ventricles.

A new integrated method for quantitating temporal and spatial systolic wall motion heterogeneity was developed and applied in 15 normal subjects and 26 patients with previous myocardial infarction (MI). After frame by frame digitizing, right anterior oblique left cineventriculograms (LV) were analyzed with 90 spaced radii. For each radius shortening fractions at sequential systolic time points relative to end diastole were correlated with corresponding normalized time points using linear regression method, yielding the radial correlation coefficient (r) and the radial regression slope (b) for temporal and spatial information. High radial r values with small standard deviations were observed in normal LV (0.972 +/- 0.016) and in non-MI regions (0.964 +/- 0.018), indicating temporally homogeneous radial shortening. A significant temporal heterogeneity in wall motion was demonstrated in MI regions (0.480 +/- 0.304) (p less than 0.001). In comparison with normal b values (0.449 +/- 0.106), there were decreased b values in MI regions (0.203 +/- 0.211) (p less than 0.001) and increased b values in non-MI regions (0.695 +/- 0.213) (p less than 0.001), suggesting hypokinetic and compensative hyperkinetic contraction in corresponding regions. Thus, temporal and spatial wall motion throughout systole could be assessed quantitatively by the present computer-assisted method with two simple integrated parameters.

Adult↗
PubMed1986

Ventricular arrhythmias and Q-Tc interval during stress-ECG.

Q-T prolongation is well-known to be related to ventricular arrhythmias in a number of clinical circumstances. The purpose of this study was to determine whether heart rate corrected Q-T interval (QTc) may indicate susceptibility to ventricular arrhythmias during stress testing. QTc was determined at rest, during submaximal and maximal bicycle work load in normals and patients with remote myocardial infarction, documented coronary artery disease (CAD) and in a group of patients with different cardiac diseases and premature ventricular beats during exercise testing (PVC). Ventricular arrhythmias were graded according to Lown. Q-Tc interval significantly increased in all groups of those patients having complex ventricular arrhythmias (Lown greater than or equal to III). In patients with ischemic S-T segment depression during stress testing, QTc was only lengthened if complex ventricular arrhythmias were present. Q-Tc lengthening in stress testing is assumed to be associated with occurrence of ventricular premature beats rather than ischemia. There is evidence that abnormal repolarization due to imbalance of the autonomic nervous system induces ventricular arrhythmias. Monitoring of Q-Tc interval during stress testing is warranted and may be useful to predict future cardiac events such as sudden cardiac death.

Angina Pectoris↗
PubMed1986

Acute effects of nitrates on left ventricular performance and energetics.

Left ventricular myocardial performance and efficiency were analyzed on the basis of two new energetic parameters in patients with coronary heart disease. The myocardial energy consumed during one cardiac cycle is related on the one hand to the work performed (E1) and on the other to the stress-time integral (E2). E1 was obtained by analysis of the pressure-volume integral divided by the left ventricular muscle mass. E2 was obtained as follows: The stress-time integral was analyzed from pressure-volume data and wall thickness using an ellipsoidal calculation model. In order to transfer the stress-time integral into energy units, the value is multiplied by a constant factor which was obtained experimentally in myothermal studies. In patients with coronary heart disease, a single dose of nitroglycerin (1.6 mg s.l.) reduced the total energy sigma (E1 + E2) from 6.1 mcal/g to 4.7 mcal/g (n = 10; P less than 0.01). The efficiency of myocardial contraction (E1/sigma (E1 + E2] was not changed significantly. These data explain quantitatively the beneficial effect of preload and afterload reduction due to nitroglycerin.

Energy Metabolism↗
PubMed1986

Hemodynamic response to LBNP following 2 hours HDT (-6 degrees).

Central hemodynamics have been determined during stepwise decreasing LBP in head-down tilt (HDT) of -6 degrees. Measurements were performed on eight healthy volunteers using right heart catheterization. During LBNP, pressures in the right atrium, pulmonary artery, and pulmonary capillary (preload) decreased in parallel with the increase of negative pressure applied to the lower part of the body. Similarly, stroke volume and cardiac output decreased with increasing negative pressure. Heart rate moderately increased (30%) as well as total peripheral resistance. The left ventricular function curve was shifted downward and to the left during LBNP indicating hypovolemia with no evidence of decreased contractility. Cardiac dimensions determined by echocardiography changed in a similar way as those obtained by invasive measurements. There was a very close correlation between stroke volume determined by thermodilution and by echocardiography. Plasma norepinephrine and dopamine tended to increase at the end of LBNP. Echocardiography proved a useful and reliable approach to hemodynamic measurement during LBNP and is recommended for analysis of hemodynamic parameters during zero G and Gz simulation.

Adult↗