Search PubMed⌕ Search

Biomedical subjects

W Motz

Publications and source records attributed to W Motz.

At least 55 records · Page 3Linked to original sources
PubMed1993

[Improvement of coronary reserve following regression of hypertrophy resulting from blood pressure lowering therapy with a beta-receptor blocker].

The coronary microcirculation was investigated by the argon gas method in ten patients (eight men, two women; mean age 56 [44-63] years) before and after an average of 12.9 (9-18) months of treatment with the cardioselective beta-receptor blocker bisoprolol. Left ventricular muscle mass was measured echocardiographically, before and after the treatment. All these patients were known to have hypertension, with exercise-related angina and ischaemic signs in the resting ECG, but normal coronary angiograms. After the treatment period both maximal coronary perfusion and coronary reserve had increased by 22%. At the same time, left ventricular muscle mass had decreased from 161 +/- 18 to 146 +/- 21 g/m2. These results demonstrate that blood pressure reducing treatment can bring about not only a regression of left ventricular hypertrophy, but also an improvement in coronary reserve.

Adult↗
PubMed1993

ACE-inhibitors in coronary artery disease?

Angiotensin converting enzyme (ACE)-inhibitors are established in the treatment of arterial hypertension and heart failure. In recent years ACE-inhibitors have also been used in the treatment of patients with coronary artery disease (CAD), since from experimental data an antiischemic action of these agents is suggested. Antiischemic effects of ACE-inhibitors may be exerted through a reduction of myocardial oxygen demand, by a reduction of angiotensin-mediated coronary vasoconstriction, by an interaction with bradykinin and the prostaglandin system, by a modulation of endothelial control of vascular tone, and by an interaction with the sympathetic nervous system. However, clinical findings on potential beneficial effects of ACE-inhibitors in patients with CAD are inconsistent and controversial. While in hypertensive patients with CAD ACE-inhibitors generally seem to attenuate myocardial ischemia at rest and during exercise, a significant fraction of about 30% of normotensive patients with CAD does not benefit or even deteriorates. Lowering of coronary perfusion pressure and alteration of transmural blood flow distribution may be responsible for this. In patients with left ventricular dysfunction (SOLVD) or congestive heart failure (CONSENSUS, SOLVD) ACE-inhibitors have been proven to prevent progressive deterioration in left ventricular function and to reduce mortality. In patients with asymptomatic left ventricular dysfunction after myocardial infarction (SAVE), long-term administration of captropril was associated with an improvement in survival and reduced morbidity and mortality due to major cardiovascular events. Therefore, from a prognostic viewpoint patients with CAD and left ventricular dysfunction or congestive heart failure should be treated with ACE-inhibitors, although the clinical use of ACE-inhibitors in patients with ongoing angina pectoris may be limited by an aggravation of angina, presumably due to critically lowering coronary perfusion pressure. Finally, ACE-inhibitors failed to prevent restenosis after successful PTCA. In conclusion, from a prognostic viewpoint patients with CAD and congestive heart failure or left ventricular dysfunction should be treated with ACE-inhibitors. In hypertensive patients ACE-inhibitors generally seem to attenuate myocardial ischemia. In normotensive patients with CAD and angina pectoris but without left ventricular dysfunction ACE-inhibitors cannot generally be recommended at present, unless the patients, which may have benefit from ACE-inhibitor treatment can be better defined.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

ACE-inhibitors and coronary microcirculation.

Arterial hypertension is the most frequent cause of a disturbance of coronary microcirculation. Inspite of having normal epicardial coronary arteries, patients with arterial hypertension often have symptoms of angina pectoris and a positive exercise tolerance test. The angina pectoris-symptoms in patients with arterial hypertension are due to functional and structural alterations of the coronary microcirculation. Consequently, an antihypertensive therapy should not only aim at lowering blood pressure and reversing myocardial hypertrophy, but also improve coronary microcirculation in order to avoid the consequences of chronic ischemia on the myocardium. Until now, only experimental studies have indicated that antihypertensive therapy can improve coronary flow reserve. To determine to what extent under clinical conditions coronary flow reserve can be improved, in hypertensive patients maximal coronary blood flow, minimal coronary resistance, and coronary reserve (Dipyridamol) were studied before and after a long-term antihypertensive treatment (9-12 months) with the ACE-inhibitor enalapril (10-20 mg/d). To assess the chronic effects rather than the acute effects of the antihypertensive pharmacon, the coronary microcirculation was studied after intermission of medical therapy for a period of 1 week. Along with a decrease in LV muscle mass by about 8%, coronary reserve was improved after enalapril by 48%. It is likely that the observed increase in coronary reserve is related to the reversal of structural vascular abnormalities at the level of the coronary microcirculation. Consequently, it seems that reparation of hypertensive remodeling of the coronary microcirculation can be induced by ACE-inhibitor therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Beta-oxidation of 1-[14C]-17-[131I]-iodo-heptadecanoic acid following intracoronary injection in humans results in similar release of both tracers.

Radioiodine labelled 17-iodo-heptadecanoic acid (IHA) is used for non-invasive study of myocardial metabolism in coronary heart disease and cardiomyopathy. Yet in the interpretation of in vivo myocardial tracer kinetics, it is controversial whether the intracellular degradation of IHA or the removal of iodide across cellular membranes is the rate-limiting step in iodide release from the myocardium. In five patients undergoing coronary sinus catheterization, a mixture of about 40 kBq of [123I] NaI was injected into the left coronary artery. During the following 15-min period, frequent blood samples were taken from the aorta and the coronary sinus. In the aqueous phase of the venous blood, 14CO2 and inorganic 131I appeared nearly in parallel, with a peak time of 4-5 min. Moreover, as shown by the AV difference, there was no significant back diffusion of IHA and no significant non-specific deiodination detectable over the period of observation. There was myocardial retention of inorganic iodide (123I) injected into the left coronary artery. The data strongly support the premise that lipid turnover through beta-oxidation is the rate-limiting step in the externally measured release of iodide after IHA injection, provided that recirculating inorganic radioactive iodide is corrected for. In addition, 15 volunteers were studied using [11C]palmitic acid and [123I]IHA using PET and dynamic planar camera scintigraphy with iodide correction. There was no significant difference between the mean values of the elimination half-times, and also no significant correlation between half-times of both fatty acids for single individuals.

Carbon Radioisotopes↗
PubMed1993

Coronary microcirculation in hypertensive heart disease: functional significance and therapeutic implications.

In arterial hypertension left ventricular hypertrophy comprises myocyte hypertrophy, interstitial fibrosis and structural alterations of the coronary microcirculation. This leads to an impairment of diastolic function of the left ventricle and coronary flow reserve despite normal epicardial arteries. Consequently, antihypertensive treatment should aim at [13] reversing myocyte hypertrophy, [14] restoring myocardial structure and [8] improving coronary flow reserve along with blood pressure normalization.

Antihypertensive Agents↗
PubMed1993

Structural and functional alterations of the intramyocardial coronary arterioles in patients with arterial hypertension.

BACKGROUND: In hypertensive patients with angina pectoris, the coronary vasodilator reserve is frequently impaired despite a normal coronary angiogram. Experimental data indicate that structural alterations of the intramyocardial coronary vasculature contribute to an increased minimal coronary resistance and a diminished coronary flow reserve. METHODS AND RESULTS: In 14 patients (10 men and 4 women) with arterial hypertension and 8 normotensive subjects, minimal coronary resistance and vasodilator reserve (dipyridamole: 0.5 mg/kg body wt, gas chromatographic argon method) were determined after the angiographic exclusion of relevant coronary artery disease. Coronary reserve was depressed in hypertensive patients (2.7 +/- 2.3 vs 4.6 +/- 1.3, P < or = .05) due to increased minimal coronary resistance (0.64 +/- 30 vs 0.24 +/- 0.055 mm Hg.min.100 g.mL-1, p < or = 0.002). In right septal biopsies, mean external arteriolar diameter (21.6 +/- 2.3 vs 17.2 +/- 2.5 microns, P < or = .001), mean arteriolar wall area (271 +/- 61 vs 172 +/- 62 microns 2, P < or = .01), percent medial wall area (69.9 +/- 4.0 vs 66.0 +/- 3.2%W, P < or = .05), mean periarteriolar fibrosis area (216 +/- 122 vs 104 +/- 68 microns 2, P < or = .05), and volume density of total interstitial fibrosis (3.6 +/- 1.8 vs 1.9 +/- 0.5Vv% fibrosis, P < or = .05) were increased in hypertensive patients compared with normotensive subjects. Minimal coronary resistance correlated with %W (r = .6, P < or = .003) and Vv% fibrosis (r = .62, P < or = .002). Left ventricular mass index (111 +/- 21 vs 97 +/- 17 g/m2, P = NS) and left ventricular end-diastolic pressure (12 +/- 6 vs 8 +/- 3 mm Hg, P = NS) did not correlate significantly with minimal coronary resistance. In multivariate analysis, both %W and Vv% fibrosis explained half of the variability of minimal coronary resistance (r2 = .5, P < or = .002). CONCLUSIONS: Structural remodeling of the intramyocardial coronary arterioles and the accumulation of fibrillar collagen are decisive factors for a reduced coronary dilatory capacity in patients with arterial hypertension and angina pectoris in the absence of relevant coronary artery stenoses.

Angina Pectoris↗
PubMed1993

Heart failure on the basis of hypertension.

Arterial hypertension leads to left ventricular hypertrophy. In proportion to increased left ventricular systolic pressure, left ventricular hypertrophy is considered to be of adaptive nature from the point of view of wall stress regulation. In the beginning, left ventricular function is normal, whereas diastolic filling is already compromised by the process of hypertrophy and altered ventricular geometry. In case of ventricular dilation and wall thinning, wall stress increases and leads to an increment in myocardial oxygen demand and a decrease of left ventricular ejection fraction. This is followed by a further decline in intrinsic myocardial contractility and a decrease in the elastic material properties of the myocardium. The structure of the myocardium is characterized by myocyte hypertrophy, a process of reactive and reparative fibrosis and alterations of the coronary microcirculation. Coronary vasodilator reserve is markedly impaired and is likely to initiate a process of malperfusion and malnutrition under increased metabolic demands. Particularly, the combined involvement of myocytes, interstitium, and intramyocardial vasculature appears to predispose to late heart failure after prolonged exposure to chronic pressure overload in arterial hypertension.

Animals↗
PubMed1992

[Chronic intermittent urokinase therapy in therapy-refractory angina pectoris].

To assess the effect of urokinase-induced reduction of fibrinogen concentration on myocardial perfusion, urokinase infusions were administered for 3 months to 24 men (mean age 59 +/- 10 years) in the inoperable end-stage of coronary heart disease with treatment-resistant angina pectoris. Initially 500,000 IU urokinase were infused i.v. daily until a fibrinogen concentration of 150-200 mg/dl was reached. Treatment was then continued as out-patients at a dosage of 500,000 IU two to four times per week. After 12 weeks the fibrinogen concentration had fallen from 348 +/- 88 to 211 +/- 52 mg/dl and plasma viscosity from 1.44 +/- 0.08 to 1.33 +/- 0.09 mPa.s (P for each less than 0.01). Up to the end of 12 weeks after the end of treatment the frequency of anginal attacks fell significantly from 3.2 +/- 1.6 to 0.7 +/- 0.4 daily (P less than 0.01), while ergometric exercise capacity increased by 76%. Thallium myocardial scintigraphy demonstrated an increased perfusion in all but three of 19 patients, global in 10, regional in 6. These results indicate that in patients with treatment-resistant angina due to coronary heart disease chronic intermittent urokinase infusion provides a promising treatment alternative.

Aged↗
PubMed1992

Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs.

Left ventricular hypertrophy (LVH) constitutes a powerful independent risk factor in hypertensive heart disease. Although initially the wall stress, i.e., left ventricular afterload, remains normal, the coronary reserve is diminished due to disturbances in the microcirculation. This is also shown in the commonly present silent ischemia episodes in Holter monitoring. LVH also causes ventricular dilation and heart failure. Apart from systolic wall stress LVH is modulated by the trophic effects of the sympathetic nervous system and angiotensin II and genetic factors. Long-term antihypertensive treatment must therefore focus on regression of both LVH and the microvascular abnormalities. A step approach for the treatment of the LVH has been recommended on the basis of the experience of this working group with calcium antagonists and ACE inhibitors, whereas the place of beta-blockers is as yet unclear. Preliminary data indicate that coronary flow rescue can also be improved after chronic antihypertensive treatment.

Antihypertensive Agents↗
PubMed1992

Pharmacotherapeutic effects of antihypertensive agents on myocardium and coronary arteries in hypertension.

Hypertensive left ventricular hypertrophy comprises myocyte hypertrophy, interstitial fibrosis and structural alterations in the coronary microcirculation. This leads to impairment of diastolic function in the left ventricle and coronary flow reserve despite normal epicardial arteries. Consequently, antihypertensive treatment should aim at (1) reversing myocyte hypertrophy, (2) restoring myocardial structure and (3) improving coronary flow reserve without lowering blood pressure. In recent years many clinical studies have shown that regression of hypertensive hypertrophy can be induced by long-term treatment with ACE inhibitors, calcium-channel blockers, beta-receptor blockers and antisympathonic drugs. However, vasodilators and diuretics, which stimulate adrenoceptor activity and increase angiotensin II levels, were found to be less effective in reversing left ventricular hypertrophy. The trophic influence of catecholamines and angiotensin II on the myocardium counteracts the effect of systolic wall stress reduction due to blood pressure lowering. As regards reversal of interstitial fibrosis, ACE inhibitors seem to be effective, because fibroblast growth was found to be stimulated by angiotensin II. Recently, clinical studies have confirmed previous experimental data that improvement in impaired coronary vasodilator reserve can be realized by long-term antihypertensive therapy. In adopting an antihypertensive treatment strategy prime consideration should be given to reversal of cardiac remodelling through restoration of myocardial structure and repair of the coronary microcirculation.

Animals↗
PubMed1992

Morphometric investigation of human myocardium in arterial hypertension and valvular aortic stenosis.

UNLABELLED: Both arterial hypertension and aortic stenosis lead to pressure overload of the left ventricle. As intramyocardial vasculature is confronted with pressure overload in hypertension but not in aortic stenosis, structural differences are to be expected in both forms of left ventricular hypertrophy. With the aid of morphometry, we investigated human myocardium from autopsied hearts from six patients with arterial hypertension and 10 controls, as well as myectomy specimens from cardiac surgery from 14 patients with aortic stenosis. Mean left ventricular myocytic diameter was significantly (P less than 0.05) increased compared with controls (12.4 +/- 1.5 microns) during hypertension (+27%) as well as aortic stenosis (+65%) (P less than 0.05). This was combined with a greater volume density of perimyocytic fibrosis (controls = 0.8 +/- 0.4 V upsilon %) during hypertension (+250%) and aortic stenosis (+587%) (P less than 0.05). Walls of intramyocardial arterioles (external diameter 20-40 and 40-80 microns) were thickened to 32% and 44% (P less than 0.05) during hypertension, but not during aortic stenosis. Compared with controls, perivascular fibrosis of these arterioles was increased by +215% and 61% (P less than 0.05), respectively, during hypertension, but not during aortic stenosis. CONCLUSIONS: Myocytic hypertrophy and increased perimyocytic fibrosis accompany intraventricular pressure overload (hypertension and aortic stenosis) in human hearts. Myocardial structure as a result of arterial hypertension, but not aortic stenosis, is also characterized by intramyocardial arteriole wall-thickening and increased perivascular fibrosis. Thus, distinct structural reaction patterns are noted in the cardiac hypertrophy associated with hypertension and aortic stenosis.

Aged↗
PubMed1992

Coronary haemodynamics in hypertensive heart disease.

Cardiac constituents affected in arterial hypertension comprise the myocardium, interstitium and coronary circulation. With regard to coronary circulation, arterial hypertension is an important risk factor in coronary artery disease, but even in the absence of coronary artery disease, hypertensive patients frequently have angina pectoris or reveal electrocardiographic abnormalities suggestive of myocardial ischaemia due to coronary insufficiency. Under clinical conditions, determination of coronary flow reserve (dipyridamole; Argon-method) allows for the evaluation of impairment of coronary regulatory reserve. In comparison to healthy normotensives, coronary haemodynamics in hypertensive patients with microvascular angina are characterized by a severely increased minimal coronary resistance and reduced maximal coronary blood flow to dipyridamole. Accordingly, coronary reserve is markedly reduced by about 40%, and metabolic, myocardial and vascular factors may be involved in this reduction. In the compensated stage of arterial hypertension, with concentric left ventricular hypertrophy, myocardial factors, such as myocyte hypertrophy, extravascular compressing forces and functional implications of impaired relaxation, as well as metabolic factors, contribute to impairment in coronary reserve to a minor extent. The reduction in coronary flow reserve is not proportional to the elevation in left ventricular muscle mass and thus the degree of left ventricular hypertrophy does not seem to determine the reduction in vasodilator reserve directly. Thus the reduction in coronary reserve seems to be primarily the consequence of an impaired vasodilating capacity of the coronary resistance vessels, as indicated by a severely increased minimum coronary resistance to dipyridamole, i.e. a severely reduced overall coronary conductance capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1992

Transient myocardial ischaemia in hypertensives: missing link with left ventricular hypertrophy.

Hypertensive patients often complain of angina pectoris in spite of a normal coronary angiogram. The aim of this study was to establish whether electrographical signs of transient myocardial ischaemia during 24-h ST Holter monitoring are associated with an increased left ventricular muscle mass. Thirty-five hypertensive patients were studied by 24-h Holter monitoring and M-mode and two-dimensional echocardiography. For control purposes nine normotensives were studied by the same protocol. Hypertensives with and without ST-segment depression did not differ in respect of blood pressure or left ventricular muscle mass (162.9 +/- 80 vs. 162.3 +/- 53 g m-2). Since both groups only showed a borderline left ventricular hypertrophy, the myocardial factor does not seem to be important for the occurrence of ST segment depression. Primary functional and structural alterations at the microcirculation level seem to be responsible for the occurrence of transient episodes of ST segment depression in the Holter electrocardiogram, indicating transient myocardial ischaemia.

Echocardiography↗
PubMed1992

The role of hypertension, left ventricular hypertrophy and psychosocial risks in cardiovascular disease: prospective evidence from blue-collar men.

Epidemiological studies have demonstrated that, compared with the population as a whole, there is increased cardiovascular morbidity and mortality among lower socio-economic groups. To explore determinants of the increased risk within this group, a prospective 6.5 year investigation of a cohort of 416 middle-aged (40.8 +/- 9.6 years) male blue-collar workers was undertaken. In addition to established somatic and behavioural risk factors, psychosocial influences that measured chronic occupational stress in terms of an imbalance between high effort and low reward were assessed. Multivariate logistic regression analysis shows that hypertension (odds ratio (o.r.) 3.85; 95% CI 1.59-9.34), left ventricular hypertrophy (o.r. 3.62; 95% CI 1.06-12.37), hyperlipidaemia (o.r. 2.55; 95% CI 1.08-6.00), status inconsistency (measuring low reward at work) (o.r. 2.86; 95% CI 1.04-7.80) and 'immersion' (measuring high intrinsic effort at work) (o.r. 3.57; 95% CI 1.22-10.47) independently contribute to the prediction of fatal or non-fatal cardiovascular events (acute myocardial infarction, stroke). Expected probabilities of cardiovascular events are clearly elevated if the combined effects of left ventricular hypertrophy and psychosocial risks are analysed. In conclusion, increased incidence of cardiovascular disease among lower socio-economic groups is explained by a co-manifestation of established risk factors including left ventricular hypertrophy (by ECG) and psychosocial factors measuring chronic stress at work.

Adult↗
PubMed1992

Reduced peripheral and coronary vasomotion in systemic hypertension.

In 53 patients with a history of arterial hypertension and 16 normotensive control subjects, coronary blood flow reserve by means of the argon method, and peripheral vascular flow reserve by means of venous occlusion plethysmography, were studied. The coronary flow reserve, expressed as the ratio of coronary vascular resistance under resting conditions to the minimal coronary vascular resistance after the administration of dipyridamole, was 4.34 +/- 0.89 in the normotensive group and 2.18 +/- 0.60 in the hypertensive group. There was no significant difference in forearm peak flow after 3 min of arterial occlusion between normotensive and hypertensive patients, while the peripheral minimal vascular resistance was significantly higher in hypertensive patients (8.8 +/- 3.8 mmHg x ml.min-1 x 100 ml-1 tissue) as compared to normotensive subjects (6.37 +/- 2.37 mmHg x ml.min-1 x 100 ml-1 tissue). Parallel to the reduction in coronary reserve, the peripheral flow reserve, expressed as the ratio of peripheral resting vascular resistance to peripheral minimal vascular resistance after 3 min of arterial occlusion, was significantly lower (P less than 0.01) in hypertensive subjects (3.85 +/- 2.28) as compared to normotensive subjects (5.31 +/- 1.72). These data suggest that in hypertensives an impaired vasodilator reserve of both coronary and peripheral microcirculation exists.

Angina Pectoris↗
PubMed1992

The role of nitric oxide in the regulation of coronary vascular resistance in arterial hypertension: comparison of normotensive and spontaneously hypertensive rats.

Nitric oxide (NO) plays an important role in the regulation of coronary vascular resistance. The aim of the present study was to evaluate the role of NO in the regulation of coronary vascular resistance in isolated hearts from normo- and hypertensive rats, which served as a model for arterial hypertension and hypertensive heart disease. Isolated hearts from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs) were perfused at constant flow, whereas the release of NO into the coronary circulation was measured simultaneously by the oxyhemoglobin technique. Bradykinin, an endothelium-dependent vasodilator, concentration-dependently decreased the coronary perfusion pressure in SHRs by 47 +/- 3% and in WKY rats by 35 +/- 6%. In parallel, the basal NO release increased in both groups, maximally by 154 and 118 pmol/min in SHRs and WKY rats, respectively. Amounts of released NO were sufficient to account for the bradykinin-induced coronary vasodilation. These data indicate that coronary resistance vessels in hearts from hypertensive compared to normotensive rats exhibit a higher sensitivity to the endothelium-dependent vasodilator bradykinin, paralleled by a higher release of NO into the coronary circulation. An enhanced endothelial NO synthesis within the coronary circulation may represent a compensatory mechanism aimed at counterregulating distinct changes in vascular reactivity occurring in arterial hypertension.

Animals↗
PubMed1992

[Prevention with vasoactive drugs].

Arterial hypertension is the most frequent cause of a disturbance of coronary microcirculation. Inspite of having normal epicardial coronary arteries, patients with arterial hypertension often have symptoms of angina pectoris and a positive exercise tolerance test. The angina pectoris symptoms in patients with arterial hypertension are due to functional and structural alterations of the coronary microcirculation. Consequently, an antihypertensive therapy should not only aim at lowering blood pressure and reversing myocardial hypertrophy, but also to improve coronary microcirculation in order to avoid the consequences of chronic ischemia on the myocardium. Until now, only experimental studies have indicated that antihypertensive therapy can improve coronary flow reserve. To determine (also under clinical conditions) if coronary flow reserve can be improved, in 30 hypertensive patients maximal coronary blood flow, minimal coronary resistance, and coronary reserve (dipyridamol) were studied before and after a long-term antihypertensive treatment (9-12 months) with an ACE-inhibitor (enalapril 10-20 mg/d), a calcium channel blocker (diltiazem 120-180 mg/d) and a beta 1-selective beta-receptor-blocker (bisoprolol 5-10 mg/d). To assess the chronic effects rather than the acute effects of the antihypertensive pharmacon, coronary microcirculation was studied after intermission of medical therapy for a period of 1 week. Along with a comparable decrease in LV muscle mass, coronary reserve was improved after enalapril by 48%, after diltiazem by 48%, and after bisoprolol by 22%. It is possible that the observed increase in coronary reserve is related to the reversal of structural vascular abnormalities on the level of the coronary microcirculation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗