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Biomedical subjects

W Motz

Publications and source records attributed to W Motz.

At least 91 records · Page 5Linked to original sources
PubMed1989

[Transient myocardial ischemia in hypertensive patients].

We wanted to determine whether there are episodes of myocardial ischemia in hypertensive patients with a normal coronary angiogram. ST-segment analysis on 24-h-Holter ECG was performed in 35 patients (18 males/17 females; mean age 54.6 +/- 10.4 years) with essential arterial hypertension (systolic/diastolic blood pressure 189.7 +/- 29/99.5 +/- 15 mm Hg). Left ventricular muscle mass (LVMM), enddiastolic volume (EDV), and the relation of mass to volume (M/V) were measured by ventriculography. Stenosis of coronary vessels was excluded by angiography in all patients. In 16 of 35 patients we observed 6.63 +/- 6.73 episodes of transient myocardial ischemia (ST-segment depressions greater than or equal to 1 mm, duration of the episode greater than or equal to 1 min). The duration of the episodes was 29.3 +/- 58.1 min, the maximal ST-segment depression 1.6 +/- 0.6 mm. In 95% of the episodes the patients did not experience any angina pectoris ("silent ischemia"). The degree of left ventricular muscle mass did not differ in hypertensive patients with and without transient myocardial ischemia (185.2 +/- 48.3 vs 227.1 +/- 71.5 g/m2). Systolic wall stress i.e. afterload was significantly higher in hypertensive patients with ST-segment depressions than in those without. In conclusion, these results demonstrate that transient myocardial ischemia often occurs in hypertensive patients. It seems that left ventricular hypertrophy by itself (myocardial factor) does not play a major role. Transient myocardial ischemia occurs mainly in hypertensive patients with eccentric myocardial hypertrophy i.e. low mass-volume ratio and high systolic wall stress. Accordingly, the occurrence of transient myocardial ischemia in hypertensive patients seems to be dependent on the myocardial energy demand.

Cardiac Volume↗
PubMed1989

[Regression of hypertrophy following nitrendipine: effect on systolic and diastolic function].

The purpose of the present study was to determine whether an antihypertensive treatment with the dihydropyridine nitrendipine can induce regression of severe hypertensive hypertrophy and, whether alterations in systolic and diastolic ventricular function do occur. Eleven patients (age 49 +/- 11 years) with hypertensive hypertrophy were treated with nitrendipine (10-40 mg/day) for 12 months. Before and after therapy left ventricular hypertrophy, systolic, and diastolic function were measured by M-mode, two-dimensional- and digitized M-mode echocardiography. Systolic blood pressure dropped from 185.5 +/- 19.8 to 164.1 +/- 15.6 mm Hg (p less than 0.05). Left ventricular muscle mass was reduced from 234.5 +/- 51.2 to 201.5 +/- 37.9 g/m2 (p less than 0.05). Systolic wall stress (257.2 +/- 50.5 vs 245.2 +/- 44.4 x 10(3) dyn/cm2) and fractional shortening (34.9 +/- 6.1 vs 37.1 +/- 5.4%) remained nearly unchanged. The peak rate of left ventricular internal dimension change during diastole (MLVD), as an index of rapid early diastolic filling was increased (13.1 +/- 3.0 vs 16.5 +/- 3.7 cm/s; p less than 0.01), the relaxation time index, as an index of isovolumic relaxation, remained nearly unchanged (76 +/- 35 vs 64 +/- 24 ms; n.s.). A long-term treatment with nitrendipine regressed hypertensive left ventricular hypertrophy in proportion to blood pressure reduction. While systolic function remained unchanged as a consequence of an unaltered systolic wall stress, i.e. afterload, diastolic filling was markedly improved due to changes in left ventricular geometry through reduction in mass to volume ratio. Since relaxation time index remained nearly unchanged, factors contributing to the phase of isovolumic relaxation were not essentially affected by regression of left ventricular hypertrophy.

Adult↗
PubMed1989

[Treatment of myocardial and coronary effects of arterial hypertension].

The hypertensive damage to the target organ "heart" comprises the sum and interactions of the cardiac organ manifestations of arterial hypertension such as myocardial hypertrophy and disease of large and small coronary arteries. 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 small coronary disease in order to improve the coronary reserve. While the evidence that regression of hypertrophy can be induced by suitable antihypertensive drugs (calcium channel blockers of the dihydropyridine type, ACE inhibitors, and sympathicolytic substances) is practically conclusive, clinical evidence of reversal of hypertensive small coronary disease has yet to be provided. Moreover, we do not know at present to what extent the prognosis of hypertensive heart disease can be improved by reversal of hypertrophy. Once the stage of hypertensive heart failure is reached, the principles of medical management of heart failure with digitalis, diuretics, and ACE inhibitors apply.

Antihypertensive Agents↗
PubMed1989

[Osteocalcin in chronic hemodialysis patients as an additional parameter in the diagnosis of advanced secondary hyperparathyroidism].

Osteocalcin (OC), also called Bone Gla Protein (BGP), is a bone matrix protein of 5800 MW synthesized by osteoblasts. Since OC is mainly metabolized in the kidney, its blood concentration is altered in renal failure. The relationship between OC and the calcium-phosphorus regulating hormones (parathyroid hormone, calcitonin) and the biochemical parameters of bone metabolism (serum calcium, serum phosphorus and serum alkaline phosphatase) was studied in 30 patients on chronic hemodialysis (mean age: 51 years; mean duration of dialysis treatment: 39 months). OC levels were significantly elevated in all patients on chronic hemodialysis (34.7 +/- 31.5 ng/ml) when compared to healthy subjects (6.25 +/- 1.39 ng/ml, p less than 0.001). In 2 patients the OC levels were excessively high (127.54 ng/ml; 148.02 ng/ml), which was associated with severe renal osteodystrophy due to secondary hyperparathyroidism. When divided into 2 groups in the patients with secondary hyperparathyroidism the mean OC value was markedly elevated (50.5 +/- 12.7 ng/ml) compared to the patients without secondary hyperparathyroidism (24.1 +/- 2.8 ng/ml) (p less than 0.05). 70 per cent of the patients on chronic hemodialysis with OC levels greater than 30 ng/ml showed moderate to severe scintigraphic findings of bone disease. In neither of the 2 groups could a correlation between OC and serum alkaline phosphatase be demonstrated. The results indicate, that OC levels could be useful additional parameter in hemodialyzed patients with secondary hyperparathyroidism and OC levels could reflect bone formation in these patients.

Adult↗
PubMed1988

[Hyperfibrinogenemia and pathological plasma viscosity. Pathogenetic factors in unstable angina pectoris?].

Plasma viscosity and erythrocyte aggregation, as the most important rheological factors in the microcirculation, and fibrinogen were measured in the blood of groups of patients in various stages of coronary-heart disease. Patients with unstable angina had viscosity and fibrinogen levels, even before any manifest infarction, that were higher than those of patients with stable angina. Plasma viscosity and hyperfibrinogenaemia (1.39 +/- 0.08 mPa.s in 48 patients and 394.4 +/- 82.7 mg/dl, respectively, in 33) were comparable to the values in patients with acute myocardial infarction (1.37 +/- 0.09 mPa.s [n = 45] and 390.2 +/- 126.9 mg/dl [n = 27], but significantly higher (P less than 0.02) than in those with stable angina (1.33 +/- 0.08 mPa.s [n = 78] and 295.3 +/- 68.6 mg/dl [n = 44], respectively). This abnormal viscosity in unstable angina plays a part in increasing myocardial ischaemia because oxygen delivery is already diminished and capillary flow slowed down. It thus contributes to progression of the angina and must be taken into account as an additional pathogenetic factor in the clinical instability.

Angina Pectoris↗
PubMed1988

[Regression of hypertensive heart hypertrophy caused by chronic angiotensin-converting enzyme inhibition].

We wanted to determine whether an antihypertensive therapy with the angiotensin-converting enzyme inhibitor enalapril can induce regression of hypertensive hypertrophy. 13 patients with hypertensive left ventricular hypertrophy were treated with enalapril (10-40 mg/day) for 9 months. Left ventricular pump function, left ventricular hypertrophy and geometry were studied by echocardiography before and 3, 6 and 9 months after enalapril treatment had been established. Both a decrease in systolic arterial blood pressure as well as a reversal of myocardial hypertrophy was obtained. After 3 months' therapy, systolic arterial blood pressure dropped from 189 +/- 8 to 171 +/- 9 mm Hg and left ventricular muscle mass decreased from 210 +/- 13 to 196 +/- 8 g/m2. After 6 months' therapy, systolic arterial blood pressure decreased further to 154 +/- 7 mm Hg and left ventricular muscle mass to 181 +/- 8 g/m2. After another 3 months' therapy (after 9 months) no further decrease in systolic arterial blood pressure (159 +/- 9 mm Hg), and no further decrease in left ventricular muscle mass (189 +/- 8 g/m2) were obtained. After 9 months' therapy, reversal of myocardial hypertrophy was adequate in relation to the amount of blood pressure lowering. Due to unaltered ventricular loading conditions, as evidenced by identical systolic wall stress values, left ventricular pump function remained unchanged.

Aged↗
PubMed1987

Blood rheology in hypertension and hypertensive heart disease.

Blood rheology was studied in 50 patients with a long history of essential hypertension, together with severe left heart hypertrophy (mass-volume relationship greater than 1.6) and angina pectoris, as well as in 17 patients with renoparenchymal hypertension. The rheologic findings were compared with those of 34 normotensive patients in whom coronary artery disease (CAD) was excluded by coronary angiography. Based on angiographic findings, the patients with essential hypertension could be differentiated into two groups: 20 hypertensive patients with normal coronary arteries and 30 hypertensive patients with coexistent CAD. In renoparenchymal hypertension, increased plasma viscosity (1.39 +/- 0.08 mPas) secondary to elevated fibrinogen levels (406.8 +/- 84.6 mg/100 ml) was found. Whole blood viscosity at low and high shear rates and the elastic component of blood were significantly more elevated in patients with renal hypertension than in patients with essential hypertension. In 30 patients with essential hypertension and coexistent CAD, higher levels of plasma viscosity (1.37 +/- 0.08 mPas, p less than 0.05) and fibrinogen (294.1 +/- 55.1 mg/100 ml, p less than 0.02) were found than in patients with essential hypertension and normal coronary arteries (1.32 +/- 0.07 mPas and 259.8 +/- 44.9 mg/100 ml, respectively). Hypertensive patients with normal coronary arteries, however, showed significantly higher levels of plasma viscosity, red blood cell aggregation, and whole blood viscosity than did normotensive controls. It is conceivable that increased blood viscosity in hypertensive patients with normal coronary arteries contributes to angina pectoris and to the reduction in coronary reserve that is observed in hypertensive patients (1).

Blood Viscosity↗
PubMed1987

Ventricular arrhythmias in hypertensive heart disease with and without heart failure.

Forty-two patients with hypertensive heart disease but without coronary macroangiopathy were examined for ventricular arrhythmias by means of 24-h, long-term electrocardiograms (ECG). They were divided into two groups according to specific criteria. Group 1 was composed of 30 patients with left ventricular hypertrophy but normal ventricular volumes, as determined by ventriculography. Group 2 comprised 12 patients with left ventricular hypertrophy and dilated left ventricles. By means of two 24-h, long-term ECGs, the mean absolute number of ventricular extrasystoles was ascertained and severity was determined according to the classification of Ryan et al. On average, patients in group 2 showed 7.830 +/- 6.579 extrasystoles, a significantly higher (p less than 0.001) number than in patients in group 1 who had 1.132 +/- 2.639 extrasystoles/24 h. Moreover, 67% of patients in group 2 had Ryan's class 4a ventricular arrhythmias (couplets) or 4b disorders (ventricular tachycardia). However, corresponding rhythm disorders could be found in only 7% of the patients in group 1. A comparison of hemodynamic parameters and ventricular arrhythmias showed that a decreasing left ventricular ejection fraction (EF, expressed in %), a decreasing mass/volume ratio (LVMM/EDV), and an increasing systolic wall stress of the left ventricle (Tsyst) are accompanied by a nearly linear increase in ventricular extrasystoles and in the severity of the ventricular arrhythmias. During long-term ECGs, nine of 10 patients with systolic wall stress of greater than or equal to 300 dyn x 10(3)/m2 showed Ryan's class 4a or 4b ventricular arrhythmias or ventricular tachycardia during programmed ventricular stimulation. However, 12 patients with normal systolic wall stress (less than or equal to 200 dyn x 10(3)/m2) showed no or only Ryan's class 1 ventricular arrhythmias. Our investigations have shown that cardiac ventricular rhythm disorders frequently occur during decompensated hypertensive heart disease, but to a lesser extent in left ventricular hypertrophy without dilation. Further investigations are needed to demonstrate whether regression of left ventricular hypertrophy is accompanied by a reduction in the incidence of ventricular arrhythmias.

Adult↗
PubMed1987

Regression of cardiac hypertrophy: experimental and clinical results.

Since left ventricular hypertrophy is considered to be a precursor of later hypertensive heart failure, a treatment that can prevent or even reverse myocardial hypertrophy is a highly desirable goal. In order to evaluate which type of antihypertensive treatment is able to induce regression of hypertensive hypertrophy, experimental and clinical studies were performed. Experimental studies were performed in spontaneously hypertensive rats (SHRs). Left ventricular hypertrophy and pumping function were studied after antihypertensive treatment with a beta-receptor blocker (metoprolol), an arteriolar vasodilator (hydralazine), and a calcium channel blocker (nifedipine) had been instituted for a period of 20-40 weeks. Patients with hemodynamically compensated hypertensive heart disease were treated with a calcium channel blocker (nifedipine), an angiotensin-converting enzyme (ACE) inhibitor (enalapril), an antisympathetic agent (clonidine), and prazosin. Comparing the amount of blood pressure reduction with the extent of hypertrophy reversal, nifedipine, prazosin, and enalapril were equipotent, whereas clonidine was most efficient in this respect. Muscle mass was overproportionally reduced in relation to blood pressure reduction following treatment with clonidine. It is likely that this was caused by lowered catecholamine levels secondary to clonidine therapy. Left ventricular pumping function was enhanced as a result of a reduction in left ventricular afterload, whereas myocardial contractility was found to be unchanged.

Animals↗
PubMed1987

Effect of intravenous nifedipine on hemodynamics and left ventricular function in acute myocardial infarction.

Twenty-one patients with acute myocardial infarction were treated 7.6 +/- 4.9 h after the onset of symptoms with intravenous nifedipine for 48-72 h. No other vasoactive medication was given. Three patients with hypertension did not respond to nifedipine and were excluded from the analysis. In the remaining 18 patients, arterial blood pressure decreased significantly, whereas the heart rate remained unchanged. The mean pulmonary artery and capillary pressure showed a slight but significant decrease. Cardiac index increased significantly. In nine patients, two-dimensional and M-mode echocardiography could be analyzed. The left ventricular ejection fraction increased significantly from 50 +/- 3% to 56 +/- 1%. There was a significant decrease in systemic peripheral resistance index, systolic wall stress, and the calculated myocardial oxygen consumption. These hemodynamic effects persisted throughout the study period. The therapy was well controllable, and there were no significant side effects. Nifedipine improves left ventricular function without an increase in myocardial oxygen demand. This effect is primarily due to afterload reduction.

Acute Disease↗
PubMed1987

Untreated hypertensives and their quality of life.

Two groups of untreated and treated subjects with persistent manifest or borderline hypertension were identified within a prospective study on cardiovascular risk in 416 middle-aged male blue-collar workers. They were compared with respect to four dimensions of quality of life: physical symptoms, mental alertness, emotional well-being and work performance. Only one symptom (nocturnal sleep disturbances) was significantly less frequent in the untreated group. Whereas short-term benefit from drug refusal seems limited, long-term costs in terms of subclinical end-organ damage are considerable. Echocardiographic findings demonstrated early stages of left ventricular hypertrophy (LVH) in one-third of the subjects with persistent borderline hypertension. Considering the role of LVH in cardiovascular mortality, results suggest that we should reinforce diagnostic and therapeutic activities in subjects with persistent borderline hypertension.

Adult↗
PubMed1986

Basis and clinical significance of regression of hypertensive hypertrophy.

The basis of every therapy in hypertensive heart disease is blood pressure normalization. However, blood pressure should be lowered through antihypertensive drugs, which can regress LV hypertrophy, increase myocardial perfusion and improve LV function depending on the stage of hypertensive heart disease. Such a step-care of hypertensive heart disease must not be understood as a therapeutic scheme, but should be considered as an attempt to cover the clinical therapy of common hypertensive cardiac complications.

Animals↗
PubMed1986

Rapid transient analysis of myosin cross-bridge kinetics in hypertrophied hearts.

Essential hypertension, with pressure overload leading to left ventricular hypertrophy, often results in coronary artery disease and congestive heart failure. The spontaneously hypertensive rat (SHR) is an attractive model for studying the effects of long-term antihypertensive therapy on the contractile properties of the myocardium. In this study we investigated differences in mechanical and biochemical characteristics of papillary muscles from SHR and normal (Wistar-Kyoto [WKY]) rats as a function of age and treatment. We found that the rate of delayed force redevelopment after rapid stretch was less in SHR than in WKY in every age group studied, even at 2 wk of age, before hypertension was evident in the SHR. In the treated SHR, blood pressure was lower, hypertrophy was reduced and the rate of delayed force redevelopment was increased compared with the untreated SHR. Finally, the pattern of myosin isoenzymes was different in treated than in untreated SHR, being shifted to more of the fast V1 and less of the slow V3 isomyosin. We conclude that long-term antihypertensive therapy not only prevents the development of left ventricular hypertrophy, but may do so by preventing the shift in myosin isoenzyme pattern normally found in hearts subjected to a long-term pressure overload.

Actomyosin↗
PubMed1986

[Hemorheologic therapy applications in coronary heart disease].

A significant correlation was found between heightened plasma viscosity and increased red blood cell aggregation and the severity of coronary artery disease. At low shear rates and exhausted vasomotion these rheological factors can cause a reversible loss of fluidity. The reduced fluidity may induce a limitation in microcirculatory flow due to the viscus resistance. Rheological treatments aim at restoration of impaired perfusion by decreasing plasma viscosity and thus diminishing red blood cell aggregation. Further therapeutic measures tend to improve red blood cell deformability. Because of limited coronary reserve in coronary artery disease hemodilution therapy is contraindicated except the cases with polyglobulia. Thrombolytic therapy in acute myocardial infarction causes a significant reduction of plasma viscosity and red cell aggregation for at least 72 hours. This improvement in blood fluidity may beneficially influence the reperfusion of ischemic areas. A therapy with orally active hemorheological drugs (pentoxifylline and buflomedil) can be discussed as an additive treatment in severe angina pectoris refractory to specific medical therapy, since these drugs increase fluidity and inhibit platelet aggregation. The defibrination may cause thrombotic and bleeding complications in the early phase of treatment. Coronary small vessel disease represents a rare type of coronary heart disease. This disease is defined by normal epicardial coronaries and reduced coronary artery reserve. In disorders of coronary microcirculation with abnormal rheology (Waldenstrom's macroglobulinemia) rheological treatment is a rational and causal therapy.

Blood Viscosity↗