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Biomedical subjects

W Motz

Publications and source records attributed to W Motz.

At least 73 records · Page 4Linked to original sources
PubMed1992

Morphometric investigation of intramyocardial arterioles in right septal endomyocardial biopsy of patients with arterial hypertension and left ventricular hypertrophy.

A reduced maximal coronary vasodilatator capacity is reported in patients with hypertensive heart disease, suggesting structural abnormalities of intramyocardial arterioles. Right septal endomyocardial catheter biopsies (EMCB) of 30 patients with arterial hypertension and of 10 heart donors were investigated morphometrically. In hypertension, the mean external diameter (21.9 +/- 3.0 vs. 17.4 +/- 2.9 microns, p less than or equal to 0.01) of arterioles and the mean arterial wall area (284 +/- 80 vs. 167 +/- 69 microns2, p less than or equal to 0.05) were increased as compared with heart donors. Perivascular fibrosis was markedly increased (260 +/- 183 vs. 41 +/- 30 microns2, p less than or equal to 0.05) as well as volume density of fibrosis (3.0 +/- 1.7 vs. 0.9 +/- 0.8 Vv%, p less than or equal to 0.01) in hypertensive heart disease. There was no significant correlation between echocardiographically determined left ventricular mass index (115 +/- 25 g/m2 for men and 104 +/- 12 g/m2 for women) and mean arteriolar wall area (r = +0.17) or volume density of fibrosis (r = +0.2) in hypertensive heart disease. Our investigations show that in patients with arterial hypertension there is a thickening of intramyocardial arteriolar walls and an increase in fibrosis. Intramyocardial vascular alterations seem to manifest in hypertension independent from left ventricular hypertrophy.

Aged↗
PubMed1992

[Dysplastic intramyocardial arteries with subaortic septum in patients with hypertrophic obstructive cardiomyopathy].

Abnormal, dysplastic intramyocardial arteries were reported in autopsied hearts of hypertrophic cardiomyopathy. To elucidate their significance, the operatively-excised myectomy specimens of 24 patients with hypertrophic-obstructive cardiomyopathy (HOCM), of 18 patients with valvular aortic stenosis and of 10 postmortem normal hearts were investigated. Eight patients with HOCM had dysplastic intramyocardial arteries (greater than 100 microns external diameter) as well as dysplastic arterioles (less than 100 microns external diameter). The value of the scores for the thickness and fibroelastosis of the media was nearly doubled, the tunica intima was frequently thickened, and the lumen was relatively reduced in dysplastic vessels. Neither in controls nor in aortic stenosis dysplastic arteries were found. Volume density of patchy fibrosis (scars) was increased in patients with dysplastic arterial vessels (HOCM II) (7.2 +/- 4.4 Vv%) (p less than or equal to 0.05) as compared with HOCM without dysplastic vessels (HOCM I) (0.8 +/- 2.3 Vv%), with aortic stenosis (0.9 +/- 1.6 Vv%) or with controls (0 Vv%), Patients with HOCM II were significantly (p less than or equal to 0.05) younger (30 +/- 13 years) than those with HOCM I (53 +/- 12 years), aortic stenosis (56 +/- 12 years), or controls (63 +/- 21 years). The anterior septum was significantly thicker in HOCM II (29 +/- 7 mm) than in HOCM I (22 +/- 4 mm), in aortic stenosis (19 +/- 3 mm), or in controls (12 +/- 2 mm). Syncopes were complained by about 75% (6/8) of patients in HOCM II, by 54% (9/16) in HOCM I, and by 44% (8/18) in aortic stenosis (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Evidence of endothelial dysfunction in coronary resistance vessels in patients with angina pectoris and normal coronary angiograms.

This study determines whether an impaired endothelium-mediated vasodilation in coronary resistance vessels exists in patients with microvascular angina. In 23 patients with clinically suspected coronary artery disease and smooth coronary arteries in the angiogram, coronary flow in response to an endothelium-related (acetylcholine) and endothelium-unrelated (dipyridamole) vasodilation was measured. Coronary flow was determined by the gas-chromatographic argon method (1) before, (2) with intracoronary acetylcholine infusion, and (3) after dipyridamole administered intravenously. In 8 patients, acetylcholine did not significantly increase coronary flow (from 91 +/- 28 to 118 +/- 37 ml/min.100 g), whereas flow was greatly increased after administration of dipyridamole (258 +/- 97 ml/min.100 g), indicating an endothelium-related vasodilator defect. In 6 patients, neither acetylcholine nor dipyridamole caused a significant increase in coronary flow, indicating an impaired coronary vasodilation on the vascular site. In 6 patients, coronary flow increased markedly after both administration of both acetylcholine and dipyridamole (from 81 +/- 26 to 191 +/- 68 and 234 +/- 87 ml/min.100 g). In 3 patients given acetylcholine, coronary artery constriction occurred. No significant correlation was found between the response to acetylcholine and that to dipyridamole (r = 0.40, p = not significant). The results indicate that in a subgroup of patients with smooth coronary arteries angina can be caused by an abnormality of the endothelial function in the microcirculation.

Acetylcholine↗
PubMed1991

Long-term treatment in arterial hypertension for protecting hypertrophic myocardium.

The cardiac organ manifestation of arterial hypertension comprises the myocardium itself with left-ventricular hypertrophy, the interstitium with perivascular and interstitial fibrosis, and the coronary circulation with disease of large and small coronary arteries. The consequences of the sum and interactions of these cardiac organ manifestations have an impact on left-ventricular systolic and diastolic function, the ischemic risk, and the occurrence of arrhythmias in hypertensive patients. As the prognosis of arterial hypertension is determined, to a considerable extent, by these cardiac complications, the aim of treatment of hypertensive heart disease is reversal of the myocardial hypertrophy in order to prevent later progression to hypertensive failure. A further goal of therapy is reversal of hypertensive coronary microangiopathy in order to improve the coronary reserve and to reduce the ischemic risk. Regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympatholytic substances). While normal systolic function was maintained in the compensated stage of hypertensive hypertrophy and was not significantly influenced by antihypertensive therapy, diastolic function was impaired in a very early stage of arterial hypertension. Both the phase of isovolumic relaxation and the phase of early diastolic filling were imparied, while after long-term antihypertensive treatment with Ca-channel blockers of the dihydropyridine type or ACE inhibitors, only the latter one was improved. From preliminary results there is clinical evidence that hypertensive disease of small coronary arteries can be reversed after long-term antihypertensive treatment with a consequently improved coronary reserve and a reduced ischemic risk. Moreover, to what extent the prognosis of hypertensive heart disease can be improved by reversal of myocardial hypertrophy and disease of small coronary arteries is yet unknown.

Cardiomegaly↗
PubMed1991

Coronary circulation in arterial hypertension.

Arterial hypertension is the most common cause of congestive heart failure and an important risk factor in coronary artery disease (CAD). However, even in the absence of CAD, coronary reserve is frequently impaired in hypertensive patients. To study whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy (LVH) or is a consequence of primary vascular alterations, coronary reserve was determined in 31 hypertensive patients (age of 56 +/- 10 years; systolic/diastolic blood pressure of 167 +/- 18/98 +/- 9 mm Hg) with angina pectoris and normal coronary angiogram. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0.5 mg/kg of body weight i.v.). Coronary blood flow was measured quantitatively by the gas chromatographic argon method. LV muscle mass was measured by ventriculography. Twelve normotensive patients (age of 52 +/- 8 years) were studied for comparison. Coronary resistance was 20% higher in hypertensive than in normotensive patients, whereas coronary blood flow at rest was not significantly different. The maximal coronary blood flow after dipyridamole was 40% lower in hypertensive than in normotensive patients; accordingly, minimal coronary resistance was significantly increased by 112% in hypertensive patients (p less than 0.0005). Coronary reserve was reduced by 37% (p less than 0.001) in hypertensive patients compared with normotensive patients. Between the impairment in coronary reserve and left ventricular muscle mass, no significant correlation (r = 0.024, n.s.) was found. The impaired coronary vasodilator reserve is reflected by episodes of transient myocardial ischemia during ST-segment monitoring.

Animals↗
PubMed1991

Coronary vascular changes in the progression and regression of hypertensive heart disease.

Coronary hemodynamics (blood flow, coronary reserve, myocardial oxygen consumption) were analyzed in both experimental and clinical hypertension. Significantly reduced coronary reserve was found in hypertensive patients with left ventricular hypertrophy. Medial hypertrophy of small coronary vessels associated with a marked increase in the wall thickness/radius ratio was considered sufficient to explain the impaired coronary flow in hypertensive left ventricular hypertrophy. After long-term pharmacotherapy, there was normalization of both medial hypertrophy and coronary reserve. This small-vessel abnormality correlates well with clinical findings in hypertensive heart disease (angina and electrocardiographic changes despite normal coronary arteriogram). Moreover, this structural adaptation of the small vessels may carry the inherent risk of an impaired oxygen supply to the hypertrophied myocardium. Thus, late cardiac failure of the hypertrophied heart in hypertension may be attributed, in part, to this microcirculation disorder. Conversely, reversal of left ventricular hypertrophy and of hypertrophy of vascular smooth muscle by specific pharmacotherapy can be considered a possible rational approach to the prevention of cardiac failure in hypertensive patients. Controlled clinical trials are needed to confirm these findings with regard to prevention of heart failure, and pharmacotherapeutic studies are necessary to define the optimal drug regimen for reversal of vascular smooth muscle hypertrophy.

Adult↗
PubMed1991

[ACE inhibition: mechanisms of cardioprotection in heart hypertrophy].

Epidemiologic studies have revealed that in arterial hypertension left ventricular hypertrophy is an important risk factor for cardiac failure. Accordingly antihypertensive therapy should aim at preventing or regressing left ventricular hypertrophy. Reduction of blood pressure does not necessarily induce reversal of left ventricular hypertrophy. Vasodilators like hydralazine and minoxidil, which lead to augmented plasma levels of norepinephrine, were not able to diminish left ventricular hypertrophy. In contrast, a sympatholytic therapy with methyldopa caused a reversal of left ventricular muscle mass. These experimental findings in spontaneously hypertensive rats led to the hypothesis that catecholamines control the onset and progression of myocardial hypertrophy mostly independent of blood pressure. This hypothesis was supported by the experimental findings, that subhypertensive dosages of norepinephrine induce left ventricular hypertrophy and that this hormone promotes alpha-receptor mediated growth of isolated myocytes. Recent studies have revealed that also the renin-angiotension-system has trophic effect on the myocardium. Clinical investigations have documented regression of cardiac hypertrophy due to antihypertensive therapy with sympatholytic drugs, ACE-inhibitors, calcium-channel blockers and beta-receptor blockers. Diuretics failed to decrease left ventricular muscle mass along with blood pressure normalization.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Disorders of coronary microcirculation and arrhythmias in systemic arterial hypertension.

Arterial hypertension is associated with an increased cardiovascular mortality and an increased risk of sudden cardiac death. Therefore, the prevalence of ventricular arrhythmias, identified on 24-hour ambulatory electrocardiographic monitoring, was analyzed in 54 patients (aged 56 +/- 10 years) with arterial hypertension and normal coronary angiograms with respect to left ventricular muscle mass, mass-to-volume ratio, systolic wall stress and coronary microangiopathy. Ventricular ectopic beats (VEBs) were assessed according to a score (modified Lown classification: 1 = no VEB, 2 = less than 30 VEB/hour, 3 = greater than 30 VEB/hour, 4 = polymorphic VEB, 5 = bigeminys, 6 = couplets, 7 = nonsustained ventricular tachycardia). Coronary blood flow was measured by the gas chromatographic argon method. Coronary reserve was determined by measuring coronary resistance before (Rcor) and after (Rmin) administration of intravenous dipyridamole (0.5 mg/kg body weight) (Cor Res = Rcor/Rmin). The frequency (p less than 0.05) and severity (p less than 0.025) of VEBs was higher in normotensive than in hypertensive patients. Although the score of VEBs did not correlate with left ventricular muscle mass (r = 0.20, difference not significant), a slight correlation with mass-to-volume ratio (r = 0.32; p less than 0.05) and systolic wall stress (r = 0.30; p less than 0.05) was found. Hypertensives with a severely reduced Cor Res (less than 2.0) had a significantly higher score of VEBs than those with a nearly normal Cor Res (greater than 3.0) (5.0 +/- 1.5 vs 3.5 +/- 1.7; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1990

Transient myocardial ischemia in hypertensive heart disease.

This study determined whether episodes of myocardial ischemia occur in hypertensive patients with normal coronary angiograms. ST-segment analysis during 24-hour Holter electrocardiography was determined in 48 patients (24 men and 24 women, mean age 54.6 +/- 10.4 years) with essential arterial hypertension (systolic/diastolic blood pressure 189.7 +/- 29/99.5 +/- 15 mm Hg). The thickness of left ventricular posterior wall and septum were measured with echocardiography. Stenosis of coronary vessels were excluded on angiography in all patients. In 24 of 48 patients, 12.8 +/- 13.8 episodes of transient myocardial ischemia (ST-segment depression greater than or equal to 1 mm, duration of the episode greater than or equal to 1 minute) were observed. The duration of the episodes was 48.1 +/- 69.93 minutes and the maximal ST-segment depression was 1.91 +/- 0.82 mm. In 95% of the episodes the patients did not experience any angina pectoris. The degree of left ventricular wall thickness did not differ in hypertensive patients with and without transient myocardial ischemia (septum thickness 11 +/- 2 mm). It is concluded that transient myocardial ischemia often occurs in hypertensive patients. Thus, left ventricular hypertrophy does not appear to play any important role. The underlying cause appears to be the impaired coronary dilation capacity, i.e., vascular alterations.

Adult↗
PubMed1990

Blood rheology as a contributing factor in reduced coronary reserve in systemic hypertension.

The influence of blood fluidity on coronary reserve in patients with essential hypertension and normal coronary arteries was examined. The coronary reserve, expressed as the ratio of coronary vascular resistance under resting conditions to the coronary vascular resistance after administration of dipyridamole, was 4.1 +/- 1.5 in 10 normotensive patients with normal coronary arteries, whereas the mean value was only 2.4 +/- 0.8 in 35 hypertensive patients. When compared with the normotensive control group the 35 hypertensive patients had significantly higher levels of hematocrit (45.9 +/- 3.7 vs 42.3 +/- 3.6; p less than or equal to 0.01) and plasma viscosity (1.39 +/- 0.07 vs 1.32 +/- 0.06 mPas; p less than 0.01). Plasma fibrinogen (291 +/- 67 vs 251 +/- 25 mg/dl) and whole blood viscosity at a shear rate of 2 s-1 (7.77 +/- 1.1 vs 7.21 +/- 1.28 mPas) and at a high shear rate of 100 s-1 (4.23 +/- 0.57 vs 3.91 +/- 0.64 mPas) demonstrated a trend without statistical significance toward higher values in hypertensive patients. When the hypertensive group was further divided according to the coronary reserve (less than 2.5, severely impaired coronary reserve; greater than 2.5 less than 3.8, moderately impaired coronary reserve), the parameters of blood fluidity clearly correlated inversely with coronary reserve. This suggests a major importance of rheologic abnormalities on impaired coronary reserve in hypertensive patients.

Angina Pectoris↗
PubMed1990

Coronary microangiopathy and cardiac hypertrophy.

Even in the absence of coronary heart disease, coronary vasodilator reserve is frequently impaired in hypertensive patients. To study, whether the reduced coronary reserve is due to the degree of left ventricular hypertrophy or is a consequence of primary vascular alterations, coronary reserve was determined in 54 hypertensive patients with angina pectoris and angiographically normal coronary arteries. Twelve normotensive persons were studied for control purposes. Coronary blood flow was measured quantitatively by the gas chromatographic argon method. Coronary reserve was determined by measuring coronary resistance before and after dipyridamole (0.5 mg (kg body weight)-1 i.v.). Left ventricular muscle mass was determined by ventriculography. In hypertensive patients, minimal coronary resistance was markedly increased by 124% and coronary reserve significantly reduced by about 38% compared with healthy normotensives. Hypertensives and normotensives did not differ with respect to myocardial oxygen consumption per unit weight myocardium (11.9 +/- 2.3 vs 11.4 +/- 2.4 ml O2 100g-1 min, n.s.) and resting coronary flow (92.1 +/- 20.8 vs 91.4 +/- 18.9 ml min-1. 100 g, n.s.). No significant correlation was found between minimal coronary resistance and coronary reserve and left ventricular muscle mass and between coronary reserve and diastolic wall stress. Accordingly, the reduced coronary regulation capacity in hypertensives does not parallel the degree of left ventricular hypertrophy and is not due to an increased myocardial oxygen consumption under resting conditions. Consequently, the impaired coronary reserve in hypertensive patients seems to be the consequence of primary microvascular lesions, which are independent of the process of left ventricular hypertrophy.

Angina Pectoris↗
PubMed1989

Left ventricular systolic resistance in rats with hypertension and hypertrophy.

Traditional indexes of ventricular performance often fail to identify differences between the normal and hypertrophied ventricle. This may not be the case for load-independent mechanical properties, elastance, and resistance. Accordingly, we derived these properties of the intact left ventricle (LV) in 25-wk-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto controls (WKY) using in-situ and isolated hearts. We found that 1) pump performance was similar in SHR and WKY, both at base line and after dextran; 2) the peak systolic elastance (Emax) was higher and theoretical maximum flow (Qmax, inverse of ventricular resistance) was lower in SHR; (3) slopes of peak isovolumetric pressure-volume and stress-strain relations were significantly higher in SHR; and 4) although end-diastolic pressure-volume relation for SHR was shifted to the right, there was no difference in end-diastolic stress-strain relations. Thus elastance in hypertrophied LV is augmented due to both an increase in muscle mass and the force-generating capacity of the myocardium. Furthermore, we propose that the decrease in Qmax seen in SHR reflects a change in certain velocity-dependent properties of the myocardium, whereas the preservation of pump performance is a result of the opposing effects of increased Emax and decreased Qmax. These observations underscore the importance of quantifying systolic resistance, together with elastance, for a better assessment of the LV as a mechanical pump.

Animals↗
PubMed1989

Left ventricular function and collagen content after regression of hypertensive hypertrophy.

To determine whether regression of hypertensive hypertrophy through blood pressure control also involves left ventricular collagen and consecutive alterations in left ventricular diastolic and systolic function, antihypertensive treatment with the calcium channel blocker nifedipine (30 mg/kg.day) was employed in 20-week-old spontaneously hypertensive rats (n = 15) for a period of 20 weeks. Age-matched (40 weeks old) untreated (n = 13) and 20-week-old spontaneously hypertensive rats representing the state before therapy (n = 14) were used for comparison. Myocardial stiffness was described by the tangent modulus Km of the elastic stiffness-stress relation. Left ventricular collagen was determined by means of hydroxyproline (OH-proline) concentration. Myocardial working capacity of the left ventricle was measured as the peak developed systolic pressure per weight unit muscle mass and systolic peak pump function as the maximum achievable cardiac output under volume loading. After the 20-week course of nifedipine treatment, systolic aortic pressure dropped from 187 +/- 11 to 144 +/- 6 mm Hg (p less than 0.001). Regression of hypertrophy was shown by a left ventricular muscle/body weight ratio of 2.13 +/- 0.18 mg/g (p less than 0.01) in the 40-week-old nifedipine-treated hypertensive rats, whereas the ratios of the 20-week-old and 40-week-old untreated spontaneously hypertensive rats were 2.3 +/- 0.30 and 2.34 +/- 0.18 mg/g, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗