Search PubMed⌕ Search

Biomedical subjects

H Just

Publications and source records attributed to H Just.

At least 91 records · Page 5Linked to original sources
PubMed1995

Ventricular tachyarrhythmias, myocardial ischemia, and sudden cardiac death in patients with hypertensive heart disease.

Hypertensive heart disease is increasingly considered to be a strong and independent risk factor for sudden cardiac death. Ventricular tachyarrhythmias in these patients are common and mainly the result of electrophysiologic abnormalities and increased electrical vulnerability of the hypertrophic myocardium. However, proarrhythmia in the hypertrophic heart often is facilitated and aggravated by electrolyte disturbances, the sympathoadrenergic tone, transient blood pressure crisis, and especially by the occurrence of myocardial ischemia. Myocardial ischemia in the setting of hypertensive heart disease may result from stenotic lesions in large and/or small coronary artery vessels and, in the absence of both, will result from the altered cellular oxygen supply and consumption in the hypertrophic myocardium. Recent studies have shown that acute and transient myocardial ischemia are common in many hypertensives, often fail to be symptomatic, and that the dynamic interaction of left ventricular hypertrophy, transient myocardial ischemia, and ventricular tachyarrhythmias may provide a crucial link for the high incidence of sudden cardiac death in patients with hypertensive heart disease.

Antihypertensive Agents↗
PubMed1995

Absence of vascular tolerance in conductance vessels after 48 hours of intravenous nitroglycerin in patients with coronary artery disease.

OBJECTIVES: We examined whether reflex neurohormonal constrictor forces attenuate the vasodilator action of nitroglycerin on large peripheral conductance vessels. BACKGROUND: Continuous nitroglycerin therapy is associated with the development of early tolerance with respect to its hemodynamic effects. It remains to be demonstrated whether vascular tolerance of large conductance vessels is an important contributory factor. METHODS: Radial artery diameter and forearm blood flow velocity were measured before and 24 and 48 h after continuous intravenous nitroglycerin infusion (0.5 microgram/kg body weight per min) in 10 patients with coronary artery disease (mean age +/- SEM 59 +/- 4 years) by using a high resolution ultrasound device. Blood flow (ml/min) was calculated from mean blood flow velocity and cross-sectional area. RESULTS: Increasing concentrations of nitroglycerin led to a dose-dependent increase in radial artery diameter (maximal +24 +/- 2%) and heart rate. Forearm vascular resistance and forearm blood flow were unchanged. After 24 and 48 h of treatment, additional nitroglycerin did not further increase radial artery diameter, indicating that the nitroglycerin-induced dilation of the radial artery was maintained and was still maximal. In addition, radial artery diameter measured before and after 48 h of nitroglycerin infusion and after withdrawal of nitroglycerin in five additional patients showed that, after withdrawal, arterial diameter returned to baseline values within 35 min. Plasma renin activity and serum aldosterone and vasopressin levels increased significantly at 24 and 48 h, accompanied by a decrease in hematocrit. CONCLUSIONS: Continuous intravenous administration of nitroglycerin exerts a sustained vasodilator effect for 48 h in large conductance vessels. Neurohormonal activation and compensatory intravascular volume expansion do not attenuate the vasodilator effects of nitroglycerin on peripheral conductance vessels during the 1st 48 h of treatment.

Adult↗
PubMed1995

Clinical evidence for the fatal interaction of ventricular tachyarrhythmias, myocardial ischemia and sudden cardiac death.

During recent years, experimental data have collected convincing evidence for the fatal interaction of myocardial ischemia, ventricular tachyarrhythmias, and sudden cardiac death. In the clinical setting, data reporting on the daily relevance of such a fatal interaction lacked until recently. However, there is now increasing evidence from autoptic studies, from the evaluation of patients who survived one episode of sudden cardiac death, from the follow-up of these patients when treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and, most recently, from studies in patients with stable and especially unstable angina pectoris suffering from Holter-documented ischemic proarrhythmia, that acute and transient myocardial ischemia play an important role for the initiation as well as the aggravation of ventricular tachyarrhythmias and out-of-hospital sudden cardiac death. The present work is directed to summarize our clinical knowledge on this topic and to indicate that preventive strategies for myocardial ischemia are the "antiarrhythmic" of choice in patients with severe coronary artery disease and evidence for ischemic proarrhythmia.

Coronary Disease↗
PubMed1995

[The aortic arch as source of thromboembolism events--significance of echocardiography diagnosis].

A 43-year-old woman presented with acute embolic occlusion of the left brachial artery. She was immediately treated by surgical embolectomy. After exclusion of other possible embolic sources, the transthoracic and transesophageal echocardiographic examination revealed a floating thrombus in the aortic arch. There-upon an aortotomy and thrombectomy was performed and showed a normal wall structure of the thoracic aorta except for a minimal ulcerated lesion of the intima at the aortic arch. This case confirms that transthoracic and transesophageal echocardiography are the diagnostic methods of choice for detecting thromboembolic sources originating in the heart or thoracic aorta.

Adult↗
PubMed1995

Effects of calcium sensitizers on intracellular calcium handling and myocardial energetics.

Calcium sensitizers may influence myocardial energetics by their action on calcium turnover and on crossbridge behavior. Using a myothermal method, the effects of the Ca2+ sensitizer EMD-53998 on calcium cycling, crossbridge behavior, and myocardial energy turnover were compared with the effects of an increase in extracellular calcium from 1.25 to 7.5 mM and with the effects of the catecholamine isoproterenol. All three inotropic interventions increased isometric force development in right ventricular rabbit papillary muscles. Relaxation time was decreased with isoproterenol, unchanged with high calcium, and increased with EMD 53998. Calcium cycling-related energy consumption, as measured by tension-independent heat, increased by 234% with high calcium, by 439% with isoproterenol, and by 77% with EMD 53998. In contrast to high calcium and isoproterenol, EMD 53998 increased economy of crossbridge cycling by increasing the force-time integral of the individual crossbridge cycle. The data indicate that EMD 53998 acts by phosphodiesterase inhibition and myofilament calcium sensitization. The latter effect is in part mediated by alteration of crossbridge behavior. Because of its effects on calcium cycling and crossbridge function myocardial energy turnover was reduced significantly with EMD 53998, whereas energy turnover was unchanged with high calcium and was increased with isoproterenol. The new calcium sensitizer levosimendan was investigated in isolated failing human myocardium. Levosimendan dose-dependently increased isometric tension. The inotropic effect was associated with increased rate of relaxation and reduced relaxation time. Measurements of intracellular calcium using the photoprotein aequorin suggest that levosimendan acts by increasing myofilament calcium sensitivity and by increasing cAMP due to phosphodiesterase inhibition. However, the contribution of the cAMP system to the action of levosimendan appears to be rather small. Therefore, the finding of a positive lusitropic effect of levosimendan may be consistent with the notion that levosimendan binds to troponin-C and increases calcium sensitivity only at high (systolic) intracellular calcium concentrations.

Adrenergic beta-Agonists↗
PubMed1994

[Increased vascular sensitivity to nitroglycerin in patients with hypercholesterolemia and peripheral endothelial dysfunction].

The effects of the endothelium-dependent vasodilator acetylcholine, the endothelium-independent vasodilator nitroglycerin and a drug which inhibits basal nitric oxide (NO) release (L-NG-monomethyl-arginine [L-NMMA]) on the diameter of the radial artery and blood flow were studied in eight patients with hypercholesterolaemia (total cholesterol: 280 +/- 9 mg/dl, age 54 +/- 3 years) and eight healthy subjects of the same age (total cholesterol 197 +/- 12 mg/dl, age 51 +/- 4 years). Arterial diameter was measured by a recently developed high resolution ultrasound technique. Increasing concentrations of acetylcholine (10(-8) to 10(-6) mol/l) produced dose-dependent increases in flow rate in the healthy subjects (maximum +150% +/- 6% at 10(-6) mol/l), but much less in the patients with hypercholesterolaemia (+24% +/- 12%). L-NMMA caused comparable reductions in forearm blood flow in both groups. Nitroglycerin increased blood flow in the hypercholesterolaemia group to a significantly greater extent (+370% +/- 69%) than in the controls (+145 +/- 62%). The effects of acetylcholine, L-NMMA and nitroglycerin on radial artery diameter did not differ significantly between the two groups. The poor response (in terms of blood flow) to acetylcholine in the hypercholesterolaemia group points to an endothelial dysfunction in the arterial microcirculation. The fact that L-NMMA caused similar reductions in forearm blood flow in the controls and hypercholesterolaemia patients alike shows that basal NO synthase activity must be comparable in the two groups and therefore cannot be held responsible for the endothelial dysfunction. This endothelial dysfunction is linked with increased responsiveness to the endothelium-independent vasodilator nitroglycerin.

Acetylcholine↗
PubMed1994

[Acute right ventricular myocardial infarct. New diagnostic and therapeutic approaches in a prognostically unfavorable disease picture].

BACKGROUND: Acute inferior myocardial infarction frequently involves the right ventricle (RV). However, very little is known on the prognostic impact of RV involvement in the in-hospital and longterm course, as well as on reliable diagnostic strategies to identify RV infarction early after admission. PATIENTS AND METHODS: In 200 consecutive patients with acute inferior myocardial infarction, we assessed on admission the prevalence and diagnostic accuracy of ST elevation in lead V4R to determine RV involvement, as well as its prognostic implications for in-hospital complications, early and late mortality and the benefit of thrombolytic therapy. Follow-up period was one to six years (mean +/- SD, 37 +/- 12 months). RESULTS: In-hospital mortality after inferior myocardial infarction was 19%, major complications occurred in 47% of patients. Presence of ST-segment elevation in V4R in 107 patients (54%) was highly predictive of RV infarction (sensitivity: 88%, specificity: 78%, diagnostic efficiency: 83%) and increased the in-hospital mortality rate from 6% to 31% (p < 0.0001) and major in-hospital complications from 28% to 64% (p < 0.0001). Cox regression analysis showed ST elevation in V4R to be independent of and superior to all other clinical variables available at the time of admission (additional risk for in-hospital mortality: 7.7; for major complications: 4.7). Thrombolysis was associated with a reduced mortality (3.7 times, p < 0.0005) and complication rate (2.4 times, p < 0.0001) only in patients with RV infarction. Post-hospital course was similar in patients with and without RV infarction. CONCLUSIONS: RV involvement during acute inferior myocardial infarction, accurately diagnosed by ST-segment elevation in V4R, is a strong, independent parameter for mortality and major in-hospital complications and may help to identify patients who will benefit most from thrombolytic therapy. Electrocardiographic assessment of RV infarction should be routinely performed in all patients admitted with acute inferior myocardial infarction.

Aged↗
PubMed1994

Torsade de pointes complicating drug treatment of low-malignant forms of arrhythmia: four cases reports.

In patients with malignant ventricular arrhythmias, antiarrhythmic therapy is known to carry a substantial risk of proarrhythmia. This risk is usually considered to be low when supraventricular arrhythmias or benign ventricular arrhythmias are considered. We were able to collect data on four patients without a history of life-threatening arrhythmias, in whom antiarrhythmic therapy was used and resulted in documented ventricular fibrillation or torsade de pointes. In Cases No. 1 and 2, atrial fibrillation was treated with either quinidine or quinidine and sotalol in combination. In both patients Holter monitoring, 4-12 h after conversion to sinus rhythm, documented the spontaneous occurrence of torsade de pointes degenerating into ventricular fibrillation and requiring DC shock for termination. In Case No. 3, atrial fibrillation was treated with sotalol and amiodarone for 2 months when incessant episodes of torsade de pointes were documented. In Case No. 4, frequent but unsustained ventricular arrhythmias were treated with amiodarone in a patient suffering dilative cardiomyopathy. After 6 days of treatment at a heart rate of 54 beats/min, a marked QT increase was associated with the occurrence of repetitive episodes of polymorphic ventricular tachycardia degenerating into ventricular fibrillation. None of the patients presented significant electrolyte abnormalities in the laboratory. A pathologic increase of the QTc-time was documented in Cases No. 1, 3, and 4. In all patients antiarrhythmic therapy was withdrawn after the proarrhythmic event and the patient became free of malignant tachyarrhythmias. Antiarrhythmic therapy also carries a considerable risk of proarrhythmia when "benign" cardiac arrhythmias are treated. The risk seems to be lower than in patients with malignant arrhythmias, however it includes the occurrence of lethal tachyarrhythmias. Special attention should be paid to the selection of antiarrhythmic agents when used in combination.

Aged↗
PubMed1994

Optimum angiographic visualization of coronary segments using computer-aided 3D-reconstruction from biplane views.

Using a biplane multidirectional isocentric X-ray system, a computer-aided simulation procedure was developed to calculate the 3D structure of the coronary arteries. The algorithm uses the geometry of the biplane X-ray system and the alignments of corresponding points of the coronary arteries in two X-ray images acquired under different viewing angles. The identification of the corresponding points is greatly simplified by the calculation and display of the intersection lines of the confocal plane with the image intensifier entrances on the computer monitor. To minimize the total number of necessary corresponding points we used Bézier curves to match the courses of the coronary segments between neighboring corresponding points. The projection of the calculated 3D structure was found to be in very good agreement with the 2D course of the coronary arteries in the angiograms. The 3D structure can be viewed on the computer screen under any desired simulated projection angle within the geometrical limitation of the X-ray gantries. The user can select views on the computer monitor with orthogonal projection angles and minimal overlapping problems caused by under- and overlying structures. The method was applied in 10 cases of elective angioplasty. Previously taken diagnostic angiograms were used to reconstruct the arterial structure and to select favorable views for the forthcoming intervention.

Cineangiography↗
PubMed1994

Assessment of endothelial modulation of coronary vasomotor tone: insights into a fundamental functional disturbance in vascular biology of atherosclerosis.

The endothelium plays a major role in modulating vascular smooth muscle tone by synthesizing and metabolizing a number of vasoactive substances. Since the endothelium is both a target for and a mediator of vascular disease, functional alterations in coronary vascular reactivity due to endothelial dysfunction might play an important integral part in the clinical presentation of coronary artery disease. Recent advances in interventional techniques including intracoronary instrumentation by Doppler catheters to measure blood flow velocities and 2-D-ultrasound catheters to evaluate arterial wall architecture during coronary angiography provided the diagnostic tools to assess endothelial vasodilator function and its relation to atherosclerotic disease. The current weight of evidence suggests that disturbances of vasomotor function of epicardial conductance vessels are fundamental to the development of atherosclerosis, and impaired endothelial vasodilation is the predominant mechanism underlying inappropriate vasoconstriction in atherosclerosis. However, endothelial vasodilator dysfunction is not only confined to atherosclerotic epicardial vessels, but may also extend into the coronary microcirculation, which does not develop overt atherosclerotic lesions, but determines coronary blood flow in the absence of hemodynamically significant stenoses. The most important factors associated with impaired endothelium-mediated dilation of the coronary microcirculation are hypercholesterolemia and advanced age. With respect to the clinical presentation of coronary artery disease, endothelial vasodilator dysfunction appears to play a causative role for triggering myocardial ischemia in stable angina pectoris, to aggravate the sequelae of acute ischemic syndromes, and might be the primary underlying mechanism in some patients with syndrome X, whereas variant angina appears to be related to a hyperreactivity of the vascular smooth muscle layer. Thus, the assessment of endothelium-mediated modulation of coronary vasomotor tone in the clinical setting offers unique and important insights into mechanisms leading to ischemic manifestations of coronary artery disease.

Coronary Angiography↗
PubMed1994

Role of calcium antagonists in progression of arteriosclerosis. Evidence from animal experiments and clinical experience. Part I. Preventive effects of calcium antagonists in animal experiments.

The quantitative predominance of free and total cholesterol over the amount of mural calcium is a most significant criterion of healthy human coronary arteries during the whole life span (0-90 years). However, this normal ratio increasingly changes as soon as arteriosclerotic alterations of the coronary walls set in. Accordingly, the mural calcium content steadily rises from fatty streaks over severe arteriosclerosis and, lastly, seems to reach a climax in plaques which caused lethal coronary infarction. Furthermore, the severe arteriosclerosis of human art. dorsalis pedis with gangrene (and amputation) is characterized by a tremendous calcium incorporation and absence of any mural cholesterol changes. Only in rare cases of human basilary plaques was a dangerous cholesterol incorporation in brain arterial wall found without significant elevation of serum cholesterol levels. The presented data indicate the existence of two different types of arteriosclerosis in one and the same patient and two basically different types of experimental coronary plaques according to their chemical composition, microscopic aspect and responsiveness to calcium antagonists: 1) the calcium type, developing in vitamin-D3-treated rats, and 2) the cholesterol type, represented by fatty coronary atheromata of cholesterol-fed rabbits. Coronary atheromata of cholesterol-fed New Zealand rabbits may be suitable models for coronary heart disease in rare cases of human familiar hypercholesterolemia. The formation of conventional human coronary artery plaques, however, essentially requires a progressive uptake of calcium, thereby representing a calcium dominated type of arteriosclerosis. Calcium antagonists specifically inhibit progredient mural calcium uptake in all experimental models of arteriosclerosis tested so far. However, neither in atheromatous arteries nor in afflicted organs (myocardium, liver, kidneys) of cholesterol-fed rabbits were we able to find any significant prevention of cholesterol accumulation by calcium antagonist.

Aging↗
PubMed1994

Continuous monitoring of acute myocardial ischemia by the implantable cardioverter defibrillator.

The present generation of implantable cardioverter defibrillators (ICDs) provides a very effective device for monitoring and treating life-threatening ventricular tachyarrhythmia. Patients at risk of sudden cardiac death who are directed to this form of treatment usually have severe coronary artery disease, previous myocardial infarction, and low ejection fraction. Progression of the underlying heart disease predisposes these patients to subsequent ischemic events, including symptomatic and asymptomatic myocardial ischemia and reinfarction, which carry a substantial risk of fatal ventricular proarrhythmia. Multipolar lead configurations presently available in the ICD appear to be effective in assessing acute myocardial ischemia as induced by exercise testing or transient coronary artery occlusion. Continuous monitoring of myocardial ischemia (COMONI) by a sophisticated, multimodal ICD appears to be feasible, may offer the means to closely supervise progression and various complications of the underlying heart disease, and may help to guide automatic or interactive antiischemic treatment.

Algorithms↗
PubMed1994

Eligibility for and benefit of thrombolytic therapy in inferior myocardial infarction: focus on the prognostic importance of right ventricular infarction.

OBJECTIVES: This study was undertaken to determine eligibility for and benefit of thrombolytic therapy in patients with acute inferior myocardial infarction with or without right ventricular involvement. BACKGROUND: Right ventricular involvement commonly complicates acute inferior myocardial infarction and is considered to have prognostic relevance. We hypothesized that the presence of right ventricular infarction, diagnosed early by ST segment elevation in the right precordial lead (V4R), may be of clinical importance in identifying patients who will benefit most from thrombolytic therapy. METHODS: We studied 200 consecutive patients with acute inferior myocardial infarction to assess the prognostic impact of right ventricular infarction in those considered eligible or ineligible for reperfusion therapy. Prognostic analyses were based on the in-hospital period and a 1- to 6-year follow-up (mean [+/- SD] 37 +/- 12 months). RESULTS: ST segment elevation in lead V4R was a reliable marker of right ventricular infarction (sensitivity 88%, specificity 78%, diagnostic efficiency 83%) in 107 patients (54%) with inferior myocardial infarction. Seventy-one eligible patients (36%) received thrombolytic therapy and had a lower mortality (8% [6 of 71]) and complication (31% [22 of 71]) rate than ineligible patients (mortality rate 25% [32 of 129], p < 0.01; complication rate 56% [72 of 129], p < 0.01). However, the overall benefit of thrombolysis was restricted to patients with right ventricular infarction complicating acute inferior myocardial infarction (with vs. without thrombolysis, respectively: mortality rate 10% vs. 42%, p < 0.005; complication rate 34% vs. 54%, p < 0.05). In the absence of right ventricular infarction, no difference was observed in the mortality (7% vs. 6%, p = NS) and major in-hospital complication (27% vs. 29%, p = NS) rates, whether or not the patient underwent thrombolytic therapy. Posthospital course over 37 +/- 12 months was not different in patients with and without right ventricular infarction but was best in all patients considered for reperfusion therapy. CONCLUSIONS: During acute inferior myocardial infarction, the right precordial electrocardiogram is a simple but promising variable to identify a subgroup of patients with an unfavorable course who will benefit most from thrombolytic therapy.

Aged↗
PubMed1994

Positive inotropism and myocardial energetics: influence of beta receptor agonist stimulation, phosphodiesterase inhibition, and ouabain.

OBJECTIVE: The aim was to study the effect of three positive inotropic interventions on myocardial force development and heat production in guinea pig papillary muscles in order to investigate the energetic consequences. METHODS: The positive inotropic agents used were epinine (beta adrenoceptor stimulation), E-1020 (phosphodiesterase inhibition), and ouabain (sodium-potassium ATPase inhibition). Heat measurements were accomplished using antimony-bismuth thermopiles, and initial heat was separated into tension dependent and tension independent heat using the butanedione-monoxime (BDM) and the shortening methods. RESULTS: Optimal concentrations of epinine, E-1020, and ouabain increased peak developed force from 20.0(SD 6.6) to 55.5(9.3) (n = 5; p < 0.01), from 20.9(9.1) to 27.2(7.2) (n = 6; p < 0.05), and from 23.4(9.2) to 44.9(18.0) mN.mm-2 (n = 6; p < 0.01), respectively. Epinine and E-1020 decreased the tension-time integral per unit initial heat, ie, the economy of isometric contraction, from 5.5(1.4) to 3.6(0.5) (p < 0.01) and from 5.5(1.4) to 3.1(0.9) N.m.s.J-1 (p < 0.01), respectively; no significant change was observed with ouabain [6.7(1.4) to 8.3(0.5) N.m.s.J-1]. The tension independent heat (calcium turnover) was measured in two different ways using BDM or shortening to abolish force production. It was increased significantly by epinine (by 141-243%), E-1020 (by 77-114%), and ouabain (by 23-38%). The first measurement in brackets is the BDM estimate, the second is the shortening estimate. From the tension-time integral and the tension dependent heat the crossbridge force-time integral was analysed: epinine and E-1020 decreased the crossbridge force-time integral from 0.46(0.16) to 0.31(0.06) pN.s (p < 0.01) and from 0.50(0.19) to 0.31(0.08) pN.s (p < 0.01), respectively, while ouabain left the force-time integral unchanged [0.59(0.27) to 0.63(0.20) pN.s]. CONCLUSIONS: (1) The inotropic effect of ouabain results from an increase in muscle activation with no change in crossbridge kinetics; (2) epinine and E-1020 increase the tension independent heat and decrease the crossbridge force-time integral, both effects reducing the overall economy; and (3) the shortening and BDM methods for measuring the tension independent heat give qualitatively similar but quantitatively different results.

Adrenergic beta-Agonists↗
PubMed1994

Functional significance of angiotensin receptors in human myocardium. Significant differences between atrial and ventricular myocardium.

We studied the effects of angiotensin (Ang) I and II in a variety of isolated human cardiac tissues contracting under physiological conditions (37 degrees C, 60 beats.min-1). Ang I and II consistently increased the peak developed force of human atrial muscles by 30-40%, an effect that was completely blocked by 10(-6) M saralasine, but not by the combination of prazosin and propranolol. However, neither Ang I or II had significant inotropic effects in right and left ventricular human preparations. We were also able to demonstrate that the positive inotropic effect of Ang II in human right atrial tissue is mediated by the AT1 receptor subtype but not the AT2 receptor subtype.

Angiotensin I↗
PubMed1994

Influence of the force-frequency relationship on haemodynamics and left ventricular function in patients with non-failing hearts and in patients with dilated cardiomyopathy.

In isolated human myocardium it was shown that a positive force-frequency relationship occurs in non-failing myocardium; however, the force-frequency relationship was found to be inverse in myocardium from failing human hearts. In order to investigate the clinical relevance of these experimental findings, the influence of heart rate changes on haemodynamics and left ventricular function was studied in eight patients without heart failure and in nine with failing dilated cardiomyopathy (NYHA II-III). Right ventricular pacing was performed at a rate slightly above sinus rate and at 100, 120 and 140 beats.min-1. Haemodynamic parameters were obtained by right heart catheterization and by high-fidelity left ventricular pressure measurements. Left ventricular angiography was performed at basal pacing rate and at 100 and 140 beats.min-1. With increasing heart rate, cardiac index increased in patients with normal left ventricular function from 2.9 +/- 0.2 to 3.5 +/- 0.21.min-1.m-2 (P < 0.01) and decreased continuously in patients with dilated cardiomyopathy from 2.6 +/- 0.1 to 2.2 +/- 0.1 l.min-1. m-2 (P < 0.05). With increasing heart rate, the maximum rate of left ventricular pressure rise increased in non-failing hearts from 1388 +/- 86 to 1671 +/- 88 mmHg.s-1 (P < 0.01) and did not change in failing hearts. Ejection fraction decreased from 27 +/- 3% to 19 +/- 2% in patients with dilated cardiomyopathy (P < 0.05) when the pacing rate was changed from 84 +/- 2 beats.min-1 to 140 beats.min-1, which was associated with a significant increase in end-systolic volume without significant changes in end-diastolic volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Comparison of diagnostic accuracy, time dependency, and prognostic impact of abnormal Q waves, combined electrocardiographic criteria, and ST segment abnormalities in right ventricular infarction.

OBJECTIVE: To determine the diagnostic and prognostic impact of abnormal Q waves in comparison to or in combination with ST segment abnormalities in the right precordial and inferior leads as indicators of right ventricular infarction during the acute phase of inferior myocardial infarction. DESIGN: Prospective study of a consecutive series of 200 patients with acute inferior myocardial infarction with and without right ventricular infarction. SETTING: Department of internal medicine, university clinic. RESULTS: Right ventricular infarction was diagnosed in 106 (57%) out of 187 patients from the results of coronary angiography, technetium pyrophosphate scanning, and measurement of haemodynamic variables or at necropsy, or both. In the acute phase of inferior infarction ST segment elevation > or = 0.1 mV in any of the right precordial leads V4-6R was the most reliable criterion for right ventricular infarction (sensitivity, 89%; specificity, 83%). Abnormal Q waves in the right precordial leads, the most specific criterion (91%) for right ventricular infarction, were superior to ST segment elevation in patients admitted > 12 hours after the onset of symptoms. Both ST segment elevation in leads V4-6R (increase in in hospital mortality, 6.2-times; P < 0.001; major complications, 2.3-times; P < 0.01) and abnormal Q waves (2.3-times, P < 0.05; 1.8-times, P < 0.05) on admission were highly predictive of a worse outcome during the in hospital period. In the presence of inferior myocardial infarction previously proposed combined electrocardiographic criteria were not better diagnostically or prognostically than ST segment abnormalities and abnormal Q waves alone. CONCLUSIONS: During the first 24 hours of inferior myocardial infarction ST segment elevation and abnormal Q waves derived from the right precordial leads are complementary rather than competitive criteria for reliably diagnosing right ventricular infarction, both indicating a worse in hospital course for the patient. In this they are better than any other previously proposed combined electrocardiographic criteria in diagnosing right ventricular infarction. Right precordial leads should be routinely monitored in acute inferior myocardial infarction.

Aged↗