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Biomedical subjects

B E Strauer

Publications and source records attributed to B E Strauer.

At least 19 recordsLinked to original sources

[The local lysis therapy of spontaneous renal artery dissection with arterial thrombosis].

A 33-year-old previously completely healthy man developed severe, at first colicky then persisting, pain in the left flank. The blood pressure was 190/110 mm Hg and he had pain over the left kidney on percussion. There was a mild leucocytosis (10,300/microliters), serum creatinine of 1.5 mg/dl and a rise in lactate dehydrogenase level to 395 U/l, while the urine was unremarkable. The pyelogram demonstrated on the left the upper calyceal system only and this very weakly. Colour Doppler ultrasound showed a massively reduced blood flow in the left renal vein while the artery was not visible. Digital subtraction angiography demonstrated eccentric narrowing of the left renal artery by an intravascular thrombus, providing the diagnosis of spontaneous renal artery dissection with thrombosis. Complete recanalization occurred after local thrombolysis with 500,000 IU urokinase over 7 hours, and subsequent administration of four times 40 mg tissue plasminogen activator over 4 hours. But the scintigram still demonstrated impaired renal function with decrease in clearance to 10% of total. The patient was still symptom-free on re-examination 16 months later, serum creatinine concentration was stable at 1.3 mg/dl and the blood pressure was normal.

Adult

[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

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

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

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

Right ventricular performance in arterial hypertension.

To investigate right ventricular function, 24 patients with arterial hypertension and five normotensive controls underwent equilibrium radionuclide ventriculography with simultaneous right heart catheterization. In normal subjects, left ventricular ejection fraction was 57 +/- 2% at rest and 71 +/- 5% on effort, and right ventricular ejection fraction (RVEF) averaged 51 +/- 5% at rest and 65 +/- 2% during exercise. Pulmonary vessel resistance (PVR) was 56 +/- 37 dyn.s.cm-5 at rest and 46 +/- 10 dyn.s.cm-5 on effort. Hypertensive patients were divided into three groups according to their left ventricular function: group 1 (n = 10) had normal left ventricular ejection fraction (LVEF) at rest and on effort (57 +/- 9%; 65 +/- 6%), in this group, right ventricular systolic reserve was reduced (RVEF 52 +/- 7% at rest, ns; RVEF 57 +/- 7% on effort, P less than 0.01 compared to controls). Pulmonary vessel resistance during exercise averaged 78 +/- 24 dyn.s.cm-5, which was significantly higher compared to controls (P less than 0.01). In group 2, left ventricular contractions were normal at rest (60 +/- 6%, ns) but deteriorated during exercise to 56 +/- 8% (P less than 0.001, compared to controls). These patients also showed a lack of right ventricular augmentation at ejection fraction (54 +/- 8% at rest, ns; 56 +/- 8% under exercise, P less than 0.05). PVR was significantly enhanced during exercise (88 +/- 40 dyn.s.cm-5, P less than 0.05 compared to controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

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

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

Electrophysiological and therapeutic implications of cardiac arrhythmias in hypertension.

UNLABELLED: Hypertension, especially if associated with left ventricular hypertrophy (LVH), is a risk factor in complex ventricular arrhythmia (VA) and sudden cardiac death (SCD). To determine the effectiveness of the clinical use of programmed ventricular stimulation (PVS) we studied 40 symptomatic hypertensive patients after excluding coronary heart disease (CHD), as characterized by dizziness and palpitation, syncope, aborted SCD and/or documented complex VA. PVS revealed a normal result, i.e. a maximum of six ventricular echobeats, in 70% (group A) and a pathological result, i.e. ventricular tachycardia (VT) or fibrillation (VF) in 30% (group B). Both groups differed significantly with respect to LV (left ventricular) muscle mass: 158 +/- 45 (A) vs. 222 +/- 112 (B) g.m-2, LVEF (left ventricular ejection fraction): 71 +/- 17% (A) vs. 47 +/- 18% (B) and LV end-systolic volume index: 34 +/- 25 (A) vs. 63 +/- 27 (B) ml.m-2. Coronary reserve was comparably reduced in both groups: 2.6 +/- 1.0 (A) vs. 2.3 +/- 0.6 (B). In 3/8 (37%) patients with aborted SCD and VT/VF the clinical VA (2/2 VT and 1/6 VF) could be induced, whereas in the remaining five patients nsVT or no complex VA was induced. The therapeutic regimen included no drugs in 30%, beta-blockers in 50%, serial drug testing in 12% and implantation of an automatic cardioverter defibrillator (AICD) in 8% of patients. Ventricular late potentials (LPs), detected by the signal averaging electrocardiogram, represent zones of delayed myocardial activation, which may become an origin of ventricular tachycardias. Three criteria constitute a positive LP: (1) QRS duration greater than 114 ms, (2) root mean square voltage of the last 40 ms less than 20 microV and (3) duration of low amplitude signal below 40 microV greater than 38 ms. To look for the prognostic value of LP in hypertension we investigated 43 hypertensive patients without evidence of CHD. All three criteria were positive in 4/43 patients (9%), three of them demonstrating inducible monomorphic VT during PVS. 17/30 patients (56%) with LVH had at least one positive criterion, whereas only one out of 13 patients without left ventricular hypertrophy (8%) had one positive criterion. Symptomatic patients presenting with syncope, aborted SCD or documented VT/VF differed significantly from patients without symptoms or complex arrhythmias in regard to all three criteria. CONCLUSION: In hypertensive heart disease clinical arrhythmias as well as the result of electrophysiological testing are closely related to left ventricular performance and hypertrophy.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged

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

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

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

Left ventricular hypertrophy, myocardial blood flow and coronary flow reserve.

In this review, the coronary haemodynamics of hypertrophic heart disease are discussed with reference to data published over the last 15 years. Coronary reserve is reduced in the presence of concentric cardiac hypertrophy, but is similar to normal in hypertrophic obstructive cardiomyopathy and aortic stenosis, despite marked left ventricular hypertrophy. A moderate decrease in coronary reserve is found in aortic incompetence and in dilated essential hypertension. In hypertensive heart disease, improvement in coronary reserve can be achieved by long-term vasodilator therapy.

Animals

[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

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