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Biomedical subjects

O M Hess

Publications and source records attributed to O M Hess.

At least 73 records · Page 4Linked to original sources
PubMed1997

[Influence of combination therapy (isosorbide dinitrate and molsidomine) on the incidence of angina pectoris in patients with coronary heart disease].

UNLABELLED: Angina pectoris in patients with severe 3-vessel-disease refractory to treatment is a challenge for the treating physician. We have therefore tested the treatment efficacy of isosorbide dinitrate combined with molidomine on the frequency of angina pectoris in patients with symptoms refractory to treatment. PATIENTS AND METHODS: 15 patients with severe coronary heart disease were included in the study. The protocol included a 2-weeks stabilisation phase, followed by a 4-weeks treatment phase with 100 mg isosorbide dinitrate in the morning as well as 8 mg slow-release molsidomine at 6 p.m. RESULTS: Initially all of the 15 patients reported about daily angina pectoris attacks. After 4 weeks of treatment 4 out of 15 patients became free of symptoms. From the other 11 patients 6 reported an improvement, 5 an unchanged frequency of attacks. DISCUSSION: Combination treatment with isosorbide dinitrate with molsidomine in a slow-release form (in the nitrate free interval) showed a distinct improvement in patients with angina pectoris refractory to treatment with reduction of complaints. The effect of the combination is possibly based on a prolonged vasodilatation of the stenosed vessels and a prolonged reduction of filling pressure (reduction of preload).

Aged↗
PubMed1997

[Anemia and heart function].

Anemia typically leads to a state of hyperkinetic circulation with tachycardia, reduced peripheral resistance, increased stroke volume chamber dilatation, and finally to the development of left ventricular hypertrophy. These changes are usually well tolerated by patients with a healthy heart. In patients with heart diseases, however, anemia may lead to deterioration of ventricular performance and to increased morbidity and mortality respectively. Specific changes in cardiac function may arise depending on the causes of anemia such as myocardial iron deposition and dilatative cardiomyopathy in hemolytic anemia or alterations of homeostasis and reduction of cardiac function in renal anemia. With respect to cardiac function the cause of anemia must be corrected as far as possible and hemoglobin kept over a level of 10 g/dl. As far as renal anemia is concerned this goal can be reached by regular administration of erythropoietin and/or iron respectively.

Anemia↗
PubMed1997

[Diuretics in the treatment of heart failure: current pathophysiological aspects].

From a pathophysiologic point of view heart failure can be divided into systolic and diastolic dysfunction. Systolic dysfunction is characterized by a decreased ejection fraction and increased chamber volume which can be typically found in young people with congestive cardiomyopathy. Diastolic dysfunction is associated with an enhanced filling pressure but with a normal systolic pump function. This disorder can be typically found in elderly patients with myocardial hypertrophy. Treatment of congestive heart failure includes. 1.) reduction of central blood volume (preload reduction) 2.) decrease of peripheral resistance afterload reduction) 3.) regression of myocardial hypertrophy (improving myocardial stiffness) 4.) maintenance of atrial contraction (atrial kick) 5.) decrease of heart rate (prolongation of diastolic filling time and increase in contractility) 6.) improvement of LV relaxation (positive lusitropic effect) and 7.) prevention of myocardial ischemia (improvement in contractility and relaxation). The primary goal of medical therapy is symptomatic improvement. Reduction in morbidity and mortality is only a secondary consideration. To achieve this goal ACE-inhibitors and in certain cases betablockers (cave: neg. inotropic action) are suited best. Additionally, digitalis-especially in the presence of atrial fibrillation- and vasodilators can be used to further improve quality of life. In the case of severe heart failure with or without atrial fibrillation oral anticoagulation is indicated to prevent systemic embolication. Diuretics are often used for symptomatic improvement but have no effect on long-term survival. Aldosterone antagonists (e.g, spironolactone) have a beneficial effect on LV remodeling and probably also on mortality. The role of endothelin antagonists and atriopeptidase inhibitors in the treatment of heart failure are not yet clear.

Adult↗
PubMed1997

Angina pectoris in patients with aortic stenosis and normal coronary arteries. Mechanisms and pathophysiological concepts.

BACKGROUND: The incidence of angina pectoris (AP) in patients with severe aortic stenosis (AS) and normal coronary arteries has been reported to be 30% to 40%. The exact pathophysiological mechanism, however, is not known. The purpose of this work was to evaluate the various hemodynamic and angiographic determinants of myocardial perfusion in 61 patients with severe AS. METHODS AND RESULTS: In a retrospective analysis, 61 patients with severe AS and without significant coronary artery disease were studied. Thirty-three patients with atypical chest pain and angiographically normal arteries served as control subjects. Patients were divided into two groups: 32 with AP and 29 without AP. Quantitative coronary angiography was performed in 59 patients and 22 control subjects. Coronary flow reserve was determined in 29 patients and 7 control subjects by use of coronary sinus thermodilution technique. Patients with AP had a lower left ventricular (LV) muscle mass, an increased LV peak systolic pressure, and increased wall stress than those without AP. Vessels of the left coronary artery were smaller and coronary flow reserve was lower in patients with AP than in those without. Inadequate L V hypertrophy with an increased wall stress was found in patients with AP but not in patients without AP. CONCLUSIONS: Myocardial ischemia in patients with severe AS can occur in the absence of coronary artery disease and appears to be due to inadequate LV hypertrophy with high systolic and diastolic wall stresses and a reduced coronary flow reserve. The cause of inadequate LV hypertrophy, however, remains unclear.

Adult↗
PubMed1997

Reduced coronary flow reserve during exercise in cardiac transplant recipients.

BACKGROUND: Coronary flow reserve (CFR) is reduced in a majority of patients after heart transplantation (HTx). Pharmacological interventions, however, provide only limited information on CFR under physiological conditions. Thus, CFR during exercise was evaluated in the present study. METHODS AND RESULTS: Coronary angiography was performed at rest and during supine bicycle exercise in 35 patients early (2 to 3 months; n = 10) or late (1 to 6 years; mean, 2.5 years; n = 25) after HTx and in 8 controls (C). CFR was determined by parametric imaging after administration of 10 mg intracoronary papaverine, during exercise, and after 1.6 mg sublingual nitroglycerin. Epicardial coronary artery size was measured by quantitative coronary angiography. CFR after papaverine was normal early (3.6 +/- 0.5 versus C, 3.6 +/- 0.7; P = NS) and late (3.8 +/- 1.3 P = NS) after HTx. During exercise, CFR was normal early (3.1 +/- 0.6 versus C, 3.9 +/- 0.9; P = NS) but decreased late (2.3 +/- 0.6; P < .01) after HTx. The increase in coronary cross-sectional area during exercise was also diminished late after HTx (14 +/- 10% versus C, 22 +/- 10%; P < .05). Both exercise-induced CFR (r = -.39, P < .05) and coronary vasodilation (r = -.44, P < .01) were inversely correlated with time after HTx. CONCLUSIONS: CFR during exercise is normal early but reduced late after HTx, whereas CFR after papaverine administration is maintained. This difference between physiological and pharmacological vasodilation suggests progressive endothelial dysfunction after HTx.

Adult↗
PubMed1997

[Function of the residual myocardium after infarct and prognostic significance].

Changes of the left ventricle after myocardial infarction are characterized by geometric, structural, and vascular alterations, which have been summarized under the term "remodeling". This process takes place in the infarct region as well as in the surviving myocardium. Depending on to the size of infarction and the degree of neurohumoral activation, the left ventricle demonstrates diastolic dysfunction which may finally lead to systolic failure. The residual myocardium develops progressive myocyte hypertrophy and interstitial fibrosis. These structural alterations are due to changes in loading conditions and stimulation of the neurohumoral system with an activation of local paracrine and autocrine factors. Myocardial function can be assessed by different non-invasive (echocardiography, radionuclide ventriculography, magnetic resonance imaging, etc.) or invasive methods (e.g., simultaneous pressure-volume measurements). "Myocardial tagging" based on magnetic resonance imaging allows the assessment of 3D-motion of the left ventricle by labelling specific myocardial regions with a rectangular grid. A systolic "wringing" motion with clock-wise rotation at the base and counter-clockwise rotation at the apex has been described in normal subjects. In the ischemic myocardium, delayed relaxation with a prolonged back-rotation (untwisting) has been reported during early diastole, whereas decreased systolic contraction with delayed diastolic rotation has been observed in non-Q-wave infarction. In patients with anterolateral aneurysms, a complete loss of systolic rotation has been demonstrated. The prognostic significance of LV "remodeling" has been emphasized by several authors: The size of infarction, LV volume, LV ejection fraction, as well as the degree of neurohumoral activation have been identified as being associated with an unfavorable clinical outcome. Yearly mortality rates have been reported to range between 15 and 17% in patients with large infarcts and marked LV dilatation and between 3 and 7% in patients with small to medium-sized infarcts.

Diagnostic Imaging↗
PubMed1997

Age dependency of left ventricular diastolic function in pressure overload hypertrophy.

OBJECTIVES: We sought to evaluate whether age is a determinant of left ventricular (LV) pressure overload hypertrophy and whether diastolic function influenced the aging process. BACKGROUND: The adaptation of the left ventricle to chronic pressure overload is a complex process of hormonal, structural and hemodynamic factors. Different responses in the elderly patients have been described. METHODS: LV biplane cineangiography, micromanometry and endomyocardial biopsies were carried out in 57 patients with pure or predominant aortic stenosis. Patients were classified into a senior (< 60 years, mean age +/- SD 46 +/- 10 years, n = 35) and an elderly (< 65 years; mean age 70 +/- 4 years, n = 22) study group. LV systolic function was evaluated from biplane ejection fraction and midwall fractional shortening, whereas diastolic function was assessed from the time constant of LV pressure decay, peak filling rate and the constant of myocardial stiffness. Biopsy samples were examined morphometrically for interstitial fibrosis, fibrous content, muscle fiber diameter and volume fraction of myofibrils. RESULTS: Gender distribution and the severity of aortic stenosis were comparable in the two patient groups. LV peak systolic and end-diastolic pressures were significantly higher in the elderly than in the senior group. LV ejection fraction and midwall fractional shortening were comparable in the two groups. The time constant of relaxation and the myocardial stiffness constant were greater in the elderly than in the senior group whereas the early peak filling rate was significantly reduced in the elderly group. Interstitial fibrosis was increased, although not significantly (p < 0.06), and fibrous content was enhanced (p < 0.001) in elderly patients with respect to the senior group. There was a linear correlation between age and myocardial stiffness (r = 0.55), p < 0.0001) and an inverse relation between age and early peak filling rate (r = 0.52, p < 0.0001). CONCLUSIONS: In the presence of a comparable degree of aortic valve stenosis, elderly patients (> 65 years) present with more severe LV hypertrophy than do senior patients (< 60 years). Therefore elderly patients have a more pronounced impairment of LV diastolic function, whereas systolic function is preserved. Thus, there is an age dependency of LV pressure overload hypertrophy that can be explained by the longer duration of pressure overload or an exhaustion of the adaptation process in the elderly.

Adaptation, Physiological↗
PubMed1997

Coronary vasomotion after percutaneous transluminal coronary angioplasty depends on the severity of the culprit lesion.

OBJECTIVES: This study sought to evaluate coronary vasomotor response to percutaneous transluminal coronary angioplasty (PTCA) and its influence on proximal and distal vessel diameters with regard to stenosis severity and coronary blood flow. BACKGROUND: Coronary vasoconstriction of the distal vessel segment has been reported after PTCA. This vasoconstrictive effect was thought to be due to balloon-induced injury of the vessel wall, with release of local vasoconstrictors or stimulation of the sympathetic system with release of catecholamines, or both. METHODS: Thirty-nine patients were prospectively studied before and after PTCA. Patients were classified into two groups according to the severity of the culprit lesion: group 1 = > or = 70% to < or = 85% diameter stenosis (n = 23); and group 2 = > 85% to < or = 95% diameter stenosis (n = 16). The coronary vessel diameter of the proximal and distal vessel segments as well as the minimal lumen diameter were determined by quantitative coronary angiography. In a subgroup of 16 patients, basal and maximal coronary flow velocity was measured before and after PTCA with the Doppler FloWire system. RESULTS: The groups were comparable with regard to age, gender, serum cholesterol levels and medical therapy. The proximal vessel segment remained unchanged after PTCA in group 1 ([mean +/- SD] 0.9 +/- 3.5%, p = 0.8) but showed vasodilation in group 2 (+13.7 +/- 3.6%, p < 0.05). However, the distal segment showed vasoconstriction in group 1 (-6.7 +/- 2.0%, p < 0.01) and vasodilation in group 2 (+31 +/- 8.0%, p < 0.01). A significant correlation was found between the change in distal vessel diameter after PTCA and stenosis severity (r = 0.61, p < 0.0001). Changes in blood flow were directly correlated to stenosis severity (r = 0.85, p < 0.002); that is, rest flow increased after PTCA in narrow lesions but remained unchanged in moderate lesions. The diameter changes in the distal vessel segment after PTCA were significantly related to flow changes (r = 0.90, p < 0.0001). Coronary distending pressure of the distal vessel segment increased significantly in both groups; however, this increase was significantly greater in group 2 than in group 1 (55 +/- 4 vs. 14 +/- 3 mm Hg, p < 0.0001). CONCLUSIONS: Coronary vasomotion of the proximal and distal vessel segments after PTCA depends on the severity of the culprit lesion; that is, vasoconstriction of the distal segment is found in patients with moderate lesions and vasodilation in those with severe lesions. Thus, vasomotion of the post-stenotic vessel segment depends on the severity of the culprit lesion and is influenced by changes in coronary flow or distending pressure, or both.

Angioplasty, Balloon, Coronary↗
PubMed1996

Circadian variations of blood pressure and heart rate early and late after heart transplantation.

Cardiac reinnervation late after heart transplantation has been reported in individual patients. As a measure for reinnervation, circadian changes in arterial blood pressure and heart rate have been used but not yet systemically evaluated in cardiac transplant recipients. Ambulatory blood pressure and heart rate monitoring was performed in 62 patients for 24 hr early (<6 months, mean 26 days, range 5-90 days, n=30) and late (> or = 6 months, mean 12 months, range 7-78 months, n=32) after heart transplantation. A loss of physiological nocturnal decline in blood pressure and heart rate was noted early after transplantation, whereas late after operation an improvement in circadian changes of blood pressure and heart rate was observed. The patients late after heart transplantation had a significant higher diastolic blood pressure. A pathological circadian blood pressure and heart rate pattern was observed in patients early after heart transplantation, which was improved late after operation. This could be explained by partial reinnervation of the heart. Diastolic hypertension late after transplantation may be due to cyclosporine treatment and/or neuroendocrine hyperactivity.

Adult↗
PubMed1996

Normalization of left ventricular nonuniformity late after valve replacement for aortic stenosis.

The aim of the present study was to evaluate nonuniformity in pressure overload hypertrophy due to aortic stenosis. Twenty patients were included in the present analysis. Ten patients with severe aortic stenosis were studied preoperatively as well as early (21 +/- 8 months) and (89 +/- 21 months) after aortic valve replacement (AVR) using left ventricular biplane angiograms, high-fidelity pressure measurements and endomyocardial biopsies. Ten normal subjects served as controls. LV systolic function was assessed from biplane ejection fraction, and diastolic function from the time constant of relaxation, the peak filling rate and the constant of myocardial stiffness. Nonuniformity was evaluated from the coefficient of variation of the time to end-systole (systolic asynchrony) and peak filling rate (diastolic asynchrony) of 12 regions in right anterior oblique and left anterior oblique projection. Ejection fraction was comparable in patients with aortic stenosis and in controls, whereas preoperatively diastolic dysfunction with prolonged relaxation and increased stiffness was present in patients with aortic stenosis and was normalized late after AVR. LV systolic asynchrony was present (>25D of controls) in 7 and diastolic asynchrony in 10 of 10 patients with aortic stenosis. Early as well as late after AVR systolic asynchrony was normalized in 9 of 10 patients. Diastolic asynchrony was present early AVR in all but one patient, although there was a significant improvement with respect to the preoperative evaluation. Late after AVR there was a normalization of diastolic asynchrony in 9 of 10 patients with aortic stenosis. Thus, it is concluded that systolic asynchrony is normalized early after AVR probably due to its load-sensitivity, whereas diastolic asynchrony persists probably due to residual LV hypertrophy with increased interstitial fibrosis and myocardial stiffness. Late after AVR, diastolic asynchrony is normalized due to structural remodeling with regression of both myocardial hypertrophy and interstitial fibrosis.

Aortic Valve↗
PubMed1996

Normalization of abnormal coronary vasomotion by calcium antagonists in patients with hypertension.

BACKGROUND: Endothelial dysfunction with a loss of endothelium-dependent vasodilation has been reported in patients with arterial hypertension. The purpose of the present study was to evaluate coronary vasomotor response to dynamic exercise in patients with coronary artery disease with and without arterial hypertension and to determine the effect of calcium antagonists on coronary vasomotion. METHODS AND RESULTS: Cross-sectional areas of a normal and a stenotic coronary vessel segment were examined in 79 patients with coronary artery disease at rest and during supine bicycle exercise (Ex). Change in luminal area after acute administration of a calcium antagonist (diltiazem or nicardipine), during exercise, and after sublingual nitroglycerin (percent change compared with rest = 100%) was assessed by biplane quantitative coronary arteriography. Patients were divided into two groups: Group 1 (control) consisted of 48 patients without (normotensive subjects, n = 30; hypertensive subjects, n = 18) and group 2 of 31 patients with (normotensive subjects, n = 15; hypertensive subjects, n = 16) pretreatment with a calcium antagonist immediately before exercise. The groups did not differ with regard to clinical characteristics or hemodynamic data measured during exercise. Mean aortic pressure at rest, however, was significantly increased in hypertensive patients compared with normotensive subjects in group 1 (103 mm Hg versus 92 mm Hg, P < .01) and group 2 (110 mm Hg versus 98 mm Hg, P < .025). In group 1, exercise-induced vasomotor response was significantly different between normotensive and hypertensive patients in normal (+20% versus +1%, P < .003) and stenotic vessels (-5% versus -20%, P < .025). However, in group 2 there was coronary vasodilation in normotensive and hypertensive patients for both normal (delta Ex +23% versus +21%, P = NS) and stenotic vessel segments (+24% versus +26%, P = NS). CONCLUSIONS: Abnormal coronary vasomotion during exercise can be observed in hypertensive patients with reduced vasodilator response in normal arteries and enhanced vasoconstrictor response in stenotic arteries. Calcium antagonists prevent the abnormal response of normal and stenotic coronary arteries to exercise in hypertensive patients and thus may compensate for endothelial dysfunction with reduced vasodilator response to exercise.

Calcium Channel Blockers↗
PubMed1996

[From left hypertrophy to heart insufficiency: hemodynamic and clinical findings].

The pathophysiology of left-ventricular hypertrophy is characterized by structural remodeling with increasing content of collagen and development of ventricular dilatation ('Gefügedilatation'). According to recent clinical view points, three stages may be distinguished: first stage, compensation, second stage, diastolic dysfunction with delayed relaxation and decrease of the passive-elastic properties, third stage, systolic and diastolic dysfunction with decreasing pump function and signs of left-ventricular failure. Diastolic dysfunction is linked to delayed rotation during isovolumetric relaxation (delayed 'untwisting') which leads to decreased ventricular filling. These changes of the myocardial adaptation process may be prevented and the vicious circle interrupted by appropriate therapeutic strategies.

Adaptation, Physiological↗
PubMed1996

Tortuosity of coronary arteries in chronic pressure and volume overload.

The role of coronary tortuosity in the pathophysiology of chronic pressure and volume overload is still unclear. A new method for measuring coronary tortuosity in patients with chronic pressure and volume overload was evaluated in 62 patients. Sixteen controls, 14 patients with arterial hypertension, and 32 patients with aortic regurgitation were included in the present analysis. The left anterior descending (LAD) and circumflex (LCX) coronary arteries were traced, and tortuosity was determined in the 30 degrees right (RAO) and 60 degrees left (LAO) anterior oblique projection. Tortuosity index (TI, %) was defined as the percent ratio of calculated shortest distance divided by total length of the coronary artery. TI was 104.1 +/- 3.2% at end-diastole in controls, 105.7 +/- 3.8% in hypertensives (P < 0.05 vs. controls), and 102.9 +/- 2.5% in patients with aortic regurgitation (P < 0.05 vs. controls, P < 0.001 vs. hypertensives). Respective values at end-systole were 107.8 +/- 4.7% in controls, 109.8 +/- 7.1% in hypertensives (ns vs. controls), and 104.3 +/- 3.3% in patients with aortic regurgitation (P < 0.001 vs. controls and vs. hypertensives). No differences were found in tortuosity between RAO and LAO projection or between LAD and LCX artery. There was a significant correlation between TI and left ventricular (LV) muscle mass, LV volume, and age. Females tended to have more tortuous vessels than males. Coronary tortuosity is more pronounced in patients with chronic pressure than with volume overload. Determinants of coronary tortuosity are gender, age, LV volume, and muscle mass. Thus, coronary tortuosity seems to play an important role as a physiologic determinant for the flow and the mechanics of the vessel wall.

Age Factors↗
PubMed1996

Time to dP/dt(max), a useful index for evaluation of contractility in the catheterization laboratory.

HYPOTHESIS: The time from onset of contraction to dP/dt(max), td, is suggested as an index of contractility in the catheterization laboratory. METHODS: We studied 22 normal patients and 18 patients with myocardial failure in the catheterization laboratory. The two groups were completely separated on the td-heart rate (HR) plane. In the normal patients, HR = 73 +/- 19 beats/min, td = 73 +/- 11 ms, and an inverse linear relation td = 109-0.49 x HR (p < 0.001) exist. In the patients with myocardial failure, despite significantly higher HR than in normal patients (HR = 93 +/- 14 beats/min) (p < 0.001), td paradoxically increased (td = 89 +/- 11 ms, p < 0.0001). CONCLUSIONS: These findings support a mathematical analysis of the left ventricular pressure (LVP) during isovolumic contraction in the time domain which shows that td and (dP/dt)/P reflect the time-dependent aspects of contraction and, hence, decrease with increasing contractility. This study shows that td, at any given HR, is a reliable index of contractility. Thus, a ready-to-use td-HR plot containing a well-based separation line can provide a reliable and simple method for determining contractility in the catheterization laboratory by examining whether a patient's td value at any HR is below (normal) or above (impaired contractility) the separation line.

Cardiac Catheterization↗
PubMed1996

Assessment of systolic and diastolic LV function by MR myocardial tagging.

Heart failure has been divided into several different forms depending on etiology, clinical course and pathophysiology of left ventricular (LV) dysfunction. Systolic and diastolic dysfunction are characterized by a reduced cardiac output with normal (= diastolic dysfunction) or depressed (= systolic dysfunction) LV pump function. New diagnostic techniques such as magnetic resonance imaging (MRI) allow to determine noninvasively LV 3D motion by labelling specific myocardial regions (= myocardial "tagging") with a rectangular or radial grid. From the deformation of this grid rotational and translational motion of the heart can be derived. A "wringing" motion of the left ventricle has been described during systole which includes a clockwise rotation at the base and a counterclockwise rotation at the apex. During diastole, an "untwisting" motion has been demonstrated. In the normal heart, diastolic "untwisting" occurs primarily during isovolumic relaxation, analogous to the systolic "wringing" which takes place mainly during isovolumic contraction. A prolongation of the "untwisting" motion was found in the hypertrophied (aortic stenosis) and hibernating myocardium. Thus, heart failure is associated with profound alterations in the mechanical function of the heart which are manifested by changes in systolic "wringing" and diastolic "untwisting" motion.

Animals↗