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Biomedical subjects

H Just

Publications and source records attributed to H Just.

At least 235 records · Page 13Linked to original sources
PubMed1989

Antiarrhythmic efficacy and tolerance of oral propafenone in patients with frequent ventricular arrhythmias: experience of a multicentre study.

In a multicentre study efficacy and safety of propafenone 450 mg day-1 and 750 mg day-1 was studied in 97 patients with frequent ventricular premature beats (VPB greater than 30 h-1). 70 patients suffered from organic heart disease, in 27 patients no organic heart disease was present during an initial work-up. After a 1-week washout period, all patients underwent 24 h Holter monitoring. Patients were then treated by propafenone 450 mg day-1 and controlled for 24 h Holter, ECG, blood pressure, blood chemistry and side-effects after 1 week of treatment. At this time, 35 patients were responders (reduction of VPB greater than 84%, of ventricular pairs greater than 90% and of ventricular tachycardia 100%). The mean reduction of VPB in all patients was 60%, of ventricular pairs 88% and of ventricular tachycardia 100%. When treatment was continued for 3 weeks 20/35 patients (56%) were still responders. The mean reduction of VPB was 83%. In 42 non-responders to 450 mg day-1 the dose was increased to 750 mg day-1. Of these patients, 17 (41%) became responders after 3 weeks of treatment; the mean reduction of VPB increased from 17% (first week, 450 mg day-1) to 63% (750 mg day-1). Ventricular pairs were reduced by 80%, ventricular tachycardia by 100%. Side-effects occurred in 11/97 patients and limited therapy in six patients. The most frequent complaints were dryness of the mouth, nausea, tiredness, headache and gastrointestinal upset. In conclusion, propafenone in a dose of 450-750 mg day-1 seems to be an effective and safe antiarrhythmic agent in the majority of patients.

Administration, Oral↗
PubMed1989

Validation of a digital angiographic model to quantitate autoregulatory vasodilation of the coronary system.

Compensatory vasodilation of the distal coronary vascular bed is the major autoregulatory mechanism in response to coronary stenosis. Using impulse response analysis (IRA) of digital angiographic time-density curves, myocardial contrast-transit was modelled as two-compartment system to obtain total coronary transit times (T) and microcirculation transit times (Tmicro) as parameters of flow (Q) divided by distribution volume (V) of the corresponding compartments. IRA parameters were compared with electromagnetic Q in eight dogs. At rest, Vmicro/V increased (P less than 0.02) from 0.69 +/- 0.08 in normal arteries (n = 25) to 0.86 +/- 0.06 in stenotic arteries (n = 24). With maximal vasodilation during hyperaemia, Vmicro/V was similar for normal (0.89 +/- 0.05; n = 19) and stenotic arteries (0.9 +/- 0.05; n = 18). There was a close linear (r = 0.88) correlation between 1/Tmicro and Q during hyperaemia. However, at rest with intact vasomotor tone, 1/Tmicro and Q were linearly related (r = 0.94; n = 12) only when Q was reduced below normal by tight stenosis; but the relationship became curvilinear in non-Q-limiting stenosed and normal arteries due to progressive decrease in Vmicro. Instead, resting 1/Tmicro demonstrated a very close linear correlation with coronary flow reserve (r = 0.95). We conclude that two-compartmental modelling of coronary contrast transit reflects stenosis-mediated autoregulatory vasodilation of the coronary microcirculation by a single measurement at rest.

Animals↗
PubMed1989

Contrasting peripheral short-term and long-term effects of converting enzyme inhibition in patients with congestive heart failure. A double-blind, placebo-controlled trial.

To discover the underlying mechanisms involved in the beneficial long-term effects of angiotensin converting enzyme (ACE) inhibitors, we investigated the systemic and peripheral effects of short- and long-term ACE inhibition in patients with chronic heart failure. After assessing the short-term effects and dose titration with cilazapril, a new long-acting ACE inhibitor, 21 patients were randomized to receive either placebo or the ACE inhibitor. Seventeen patients completed the 3-month treatment. Central hemodynamic output, femoral blood flow (measured by thermodilution), oxygen saturation, and lactate and norepinephrine levels were determined simultaneously in the femoral vein and radial artery during treatment and after a 3-month rest and during symptom-limited bicycle exercise. Short-term ACE inhibition improved rest and exercise hemodynamic output, but it did not alter peak femoral blood flow, calculated leg oxygen consumption, or systemic oxygen uptake during exercise, despite significant reduction in femoral norepinephrine extraction and arterial angiotensin levels during exercise. In contrast, long-term ACE inhibition further improved exercise cardiac output and increased leg blood flow (from 2.3 to 2.9 l/min, p less than 0.05), leg oxygen consumption (from 277 to 403 ml/min, p less than 0.05), and systemic oxygen uptake (from 1,133 to 1,453 ml/min, p less than 0.05), whereas these variables remained unchanged with placebo treatment (p less than 0.02 between groups). Moreover, a moderate but significant increase in femoral oxygen extraction occurred after long-term therapy (ACE inhibitor: from 76% to 83%, p less than 0.05; placebo: from 75% to 74%, NS; p less than 0.01 between groups). We conclude that long-term ACE inhibition is clinically beneficial in that it improves blood flow to skeletal muscle during exercise over time. The long-term effects of ACE inhibition are, in part, probably related to peripheral (vascular) mechanisms, for example, by reversing the inability of peripheral vessels to dilate and by improving oxygen utilization.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Atrial natriuretic peptide in a rat model of cardiac failure. Atrial and ventricular mRNA, atrial content, plasma levels, and effect of volume loading.

This study examined the relation between synthesis, atrial storage, and plasma levels of atrial natriuretic peptide (ANP), and it examined plasma ANP levels and hemodynamic output in response to volume expansion in a rat model of myocardial infarction and failure. Arterial ANP concentrations did not correlate linearly with infarct size, but they did show an abrupt increase when infarct size exceeded 30% of the left ventricle, similar to the abrupt increase of left ventricular end-diastolic pressure with infarct size greater than 30%. Consequently, a close relation was found between plasma ANP levels and left ventricular end-diastolic pressure (n = 23, r = 0.89, p less than 0.001). Atrial ANP content per gram of tissue but not ANP content per pair of atria was reduced in rats with large infarcts (greater than 40%, p less than 0.05 vs. control animals). ANP mRNA level per pair of atria (related to total atrial RNA), determined by liquid hybridization (controlled by northern blot analysis), was increased by 38% in infarcted rats (p less than 0.05 vs. controls), but the ratio of atrial ANP mRNA relative to atrial beta-actin mRNA levels was not increased. Right and left ventricular ANP mRNA level increased by 90% and 380%, respectively, far exceeding the concomitant increase in beta-actin mRNA (+26% in the left ventricle). Plasma ANP increased with volume loading in controls and rats with moderate infarcts but not in rats with large infarcts despite a similar increase in right atrial pressure (compared with control animals); thus, the relation of delta ANP/delta right atrial pressure exerted by volume loading decreased in rats with large infarcts. Similarly, the response of cardiac output and renal blood flow (determined by radioactive microspheres) to volume loading was attenuated in rats with large infarcts. Thus, in this model of chronic cardiac failure, the activation of the ANP system is closely coupled with the increase in intracardiac pressures without correlating linearly to the extent of myocardial loss. Second, in severe cardiac failure, additional stimulation such as volume loading may elicit only an attenuated ANP secretion response, for example, due to saturation of the ANP receptor sensing system or to a limited transformation rate of pro-ANP. Third, the increase in atrial ANP synthesis and the increase in atrial ANP gene expression seems limited; however, substantial specific ANP gene expression occurs in the ventricles, which, in turn, may contribute to increased plasma ANP levels in chronic heart failure.

Animals↗
PubMed1989

Myocardial energetics in patients with dilated cardiomyopathy. Influence of nitroprusside and enoximone.

Cardiotonic agents influence myocardial energy consumption by vasodilation, which may reduce energy demand, and by inotropism, which may increase it. To distinguish between the two effects, myocardial oxygen consumption must be analyzed in relation to its hemodynamic determinants. The coupling of myocardial oxygen consumption with its determinants was investigated in 22 patients with idiopathic dilated cardiomyopathy (NYHA Class II and III). Predicted myocardial oxygen consumption by the pressure-work index, the Bretschneider index, and the pressure-volume area correlated moderately with measured myocardial oxygen consumption (r = 0.57, p less than 0.001; r = 0.52, p less than 0.005; and r = 0.63, p less than 0.001). Multiple regression analysis, including left ventricular peak systolic wall stress, systolic stress-time integral, pressure-volume work, maximum rate of left ventricular pressure rise, and mean velocity of circumferential fiber shortening indicated that systolic stress-time integral is the major determinant of myocardial oxygen consumption (r = 0.75, p less than 0.001) in these patients. Enoximone, a phosphodiesterase inhibitor, has an inotropic and a vasodilating effect. To investigate the inotropic portion of the energy cost of this phosphodiesterase inhibitor, the influence of enoximone on myocardial oxygen consumption and systolic stress-time integral was compared with the effects of nitroprusside, which is a vasodilator only. Nitroprusside (10 patients) and enoximone (12 patients) reduced left ventricular systolic stress-time integral from 109 +/- 22 to 71 +/- 21 (p less than 0.005) and from 104 +/- 23 to 42 +/- 10 (p less than 0.001) 10(3) dynes.sec/cm2, respectively. Myocardial oxygen consumption decreased from 159 +/- 44 to 112 +/- 23 (p less than 0.005) and from 134 +/- 28 to 109 +/- 21 (p less than 0.001) microliters/beat/100 g, respectively. In both groups, there was a significant correlation between the decrease in myocardial oxygen consumption and the decrease in systolic stress-time integral. The slopes of the respective linear regression lines were significantly different (1.27 for nitroprusside and 0.51 nl.cm2/100 g.dynes.sec for enoximone, p less than 0.05), indicating a smaller decrease of myocardial oxygen consumption for a given decrease of stress-time integral with enoximone. Applying the pressure-work index or the pressure-volume area instead of systolic stress-time integral yielded comparable results. Thus, vasodilation reduces myocardial oxygen consumption in proportion to the reduction of stress-time integral. With enoximone, the energy-saving effect of vasodilation is counteracted in part by the increased energy d

Adult↗
PubMed1989

Flow-dependent coronary artery dilatation in humans.

To determine the role of endothelium-mediated flow-dependent coronary dilatation in humans, we studied the coronary dilatation exerted by maximal pharmacologic increase of coronary flow in 14 patients with normal coronary arteries. Biplane views of the circumflex (Cx) and left anterior descending (LAD) coronary arteries were obtained before and 80 seconds after inducing a maximal increase in flow selectively in the Cx by injecting 7 mg papaverine through a 2F infusion catheter in the midportion of the Cx (n = 10). The diameter of the proximal Cx segment (exposed to increased flow but not to papaverine directly) increased with papaverine by 11.1 +/- 4% (range, 5.2-16.4%, p less than 0.001 vs. control), whereas the LAD diameter did not change. LAD and Cx diameters increased by 18.3% and 21.2% after nitroglycerin given into the left main artery, which showed the preserved capability of the LAD to dilate. In four patients with normal coronary arteries and six patients with coronary artery disease (CAD, non-flow-limiting stenosis), a similar protocol was applied with the LAD for the assessment of flow-dependent dilatation. Simultaneously, intracoronary blood flow velocity was measured by an intracoronary Doppler catheter. Papaverine-induced coronary flow reserve (peak/resting velocity ratio) in the LAD was 4 +/- 0.7 (range, 3.5-5) in normal arteries and was 3.5 +/- 0.6 (range, 2.7-4.4) in CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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

Influence of the positive inotropic substance pimobendan (UD-CG 115 BS) on contractile economy of guinea pig papillary muscles.

Using antimony-bismuth myothermal equipment, we measured simultaneously the initial heat liberated from and the stress-time integral developed by guinea pig papillary muscles before and after application of UD-CG 115 BS (200 microM) at an experimental temperature of 21 degrees C. By means of the shortening method, the initial heat was subdivided into the activation heat, which is associated with the calcium turnover, and the tension-dependent heat, which represents the ATP splitting by contractile proteins. The activation heat increased slightly but not significantly from 0.24 +/- 0.05 to 0.34 +/- 0.09 mcal/g. The increase in the tension-dependent heat (from 0.23 +/- 0.07 to 0.49 +/- 0.22 mcal/g) was directly proportional to the increase in the developed stress-time integral (from 0.95 +/- 0.24 to 2.37 +/- 0.76 g.s/mm2). The data indicate that the economy of force generation by contractile proteins is unchanged by UD-CG 115 BS, whereas the activation heat may be slightly increased by this compound. A comparison of UD-CG 115 BS with other substances like isoproterenol or classic phosphodiesterase inhibitors reveals that UD-CG 115 BS increases myocardial force in a more economical way that may have clinical implications. The mode of action of this compound is attributed to its calcium-sensitizing effect on the contractile proteins.

Animals↗
PubMed1989

Effects of pimobendan on hemodynamics and myocardial energetics in patients with idiopathic dilated cardiomyopathy: comparison with nitroprusside.

The influence of pimobendan and nitroprusside on hemodynamics was investigated in nine patients with idiopathic dilated cardiomyopathy (NYHA class II-III). Pimobendan and nitroprusside resulted in a comparable decrease of left ventricular end-diastolic wall stress (preload) by 46% (p less than 0.01) and 52% (p less than 0.01), respectively, and of end-systolic wall stress (afterload) by 36% (p less than 0.01) and 34% (p less than 0.01), respectively. Cardiac index increased from 3.2 +/- 0.4 to 4.2 +/- 0.8 L/min/m2 with pimobendan (p less than 0.01) and did not significantly change with nitroprusside (3.0 +/- 0.6 L/min/m2). Compared to nitroprusside, pimobendan resulted in a significant increase in stroke volume index by 37% (p less than 0.01) and maximum rate of left ventricular pressure rise by 23% (p less than 0.05). Heart rate did not significantly change with either drug. Following the application of pimobendan, there was a decrease in myocardial oxygen consumption from 14.3 +/- 5.1 to 10.6 +/- 3.8 ml/min/100 g (p less than 0.05). The ratio of myocardial oxygen consumption and systolic stress-time integral did not significantly change. Thus, in comparison with nitroprusside, pimobendan exhibits significant inotropic and vasodilating properties. The hemodynamic actions of pimobendan are associated with favorable effects on myocardial energetics.

Adult↗
PubMed1989

Influence of enoximone on mechanics and energetics of right ventricular guinea pig papillary muscles.

Using highly sensitive antimony-bismuth thermopiles, the heat that is liberated during isometric contraction (initial heat) was measured simultaneously with the force signal in right ventricular papillary muscles of guinea pigs (n = 10). Measurements were taken before and after application of enoximone in a concentration of 10(-5) M. Enoximone increased peak developed tension from 1.92 +/- 0.98 to 2.81 +/- 1.11 g/mm2 (p less than 0.01) and the tension-time integral from 1.52 +/- 0.87 to 1.86 +/- 0.86 g.s/mm2 (p less than 0.05). Initial heat was increased from 0.50 +/- 0.13 to 0.79 +/- 0.24 mcal/g (p less than 0.01). The ratio between initial heat and tension-time integral, which is an inverse measure of myocardial economy of force generation, was increased from 3.77 +/- 1.17 to 4.66 +/- 1.49 mucal/g.s.cm (p less than 0.05). To study the potential changes induced by enoximone on an intracellular level, the initial heat was separated into tension-dependent heat (cross-bridge cycling) and tension-independent heat (calcium cycling). The latter increased from 0.20 +/- 0.05 to 0.28 +/- 0.09 mcal/g (p less than 0.05). The tension-dependent heat as normalized for a unit of developed tension-time integral increased from 2.17 +/- 0.63 to 2.86 +/- 0.79 mucal/g.s.cm (p less than 0.01). From these data, we conclude that enoximone decreases the economy of myocardial force generation by (a) increasing the number of calcium ions cycling during one twitch and (b) by altering the fundamental mechanisms of the contractile proteins with respect to force generation, i.e., faster contraction velocity and decreased economy of force generation.

Animals↗
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

[Echocardiographic diagnosis of pathologic processes of the central pulmonary vessels].

Diseases of the central pulmonary arteries are difficult to diagnose. Echographic imaging of the pulmonary arteries can best be done using the suprasternal and transesophageal approach. In pulmonary arterial hypertension, the central pulmonary arteries increase in size, a fact that is used echographically to diagnose pulmonary hypertension. Even when there is volume overload (e.g. in congenital heart disease with a left-to-right shunt), characteristic changes of the pulmonary vessels are observed. Thromboemboli within the pulmonary arteries or thrombotic occlusion and a malignant process, which can lead to an obstruction or compression of the central pulmonary arteries, could be seen with echographic imaging techniques.

Arterial Occlusive Diseases↗