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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
PubMed1995

[Acute myocardial ischemia in spontaneous coronary artery spasm].

AIM OF STUDY: To discover what factors indicate spontaneous coronary artery spasms as a cause of myocardial ischaemia. PATIENTS AND METHOD: In a retrospective analysis 15 of 1407 consecutive patients who had undergone coronary arteriography (six women and nine men; mean age 47 +/- 11 years) had acute ischaemia due to spontaneous coronary artery spasms. The clinical findings at the time of first investigation and during the follow-up period (mean of 29 [3-65] months) were evaluated. RESULTS: The most common risk factors were hypercholesterolaemia (> or = 200 mg/dl) in ten patients (66%) and heavy nicotine consumption > or = 20 cigarettes per day) in eight patients (55%). Of the patients with angina at rest nine had reversible ST elevations, six had terminal T negativity in the ECG and an increased incidence of ventricular arrhythmias (n = 6). At time of hospitalization ten patients had acute myocardial ischaemia and five had signs of acute myocardial infarction (maximal creatine kinase concentration: 121-2980 U/l). Acute coronary angiography revealed circumscribed coronary artery constriction, reversible with nitroglycerin, with stenosis of < 70% in five patients and of > or = 70% in six, as well as intermittent vessel occlusion in four patients. Angiography showed smooth coronary artery walls in almost all instances. Angiographic evidence of circumscribed arteriosclerotic lesion with maximally 50% narrowing was present in six patients. CONCLUSION: Especially in younger, male patients with hypercholesterolaemia and heavy smoking recurrent anginal pectoris at rest, with reversible ECG signs of myocardial ischaemia but without advanced coronary sclerosis, speaks for spontaneous coronary artery spasms as the cause.

Acute Disease↗
PubMed1995

Response of hypertensive left ventricular hypertrophy and coronary microvascular disease to calcium antagonists.

Hypertensive left ventricular hypertrophy comprises not only myocyte hypertrophy, but is often associated with interstitial fibrosis and structural alterations of the coronary microcirculation. The consequences are early diastolic dysfunction and often later systolic dysfunction of the left ventricle, resulting in congestive heart failure. Involvement of the coronary resistance vessels leads to an impairment of coronary flow reserve despite normal epicardial arteries. Therefore, antihypertensive treatment should aim at reversing myocyte hypertrophy, restoring myocardial structure, and improvement in coronary flow reserve apart from blood pressure lowering. Many clinical studies have shown that calcium antagonists are effective in lowering blood pressure and can induce regression of left ventricular hypertrophy. Moreover, experimental studies have shown a restoration of myocardial structure. Recent clinical studies have demonstrated a marked improvement of the impaired coronary vasodilator reserve in hypertensive patients after long-term treatment with calcium antagonists. In summary, calcium antagonists can be regarded as an antihypertensive treatment modality that is able to restore myocardial structure and to repair coronary microcirculation and therefore can be considered as causative treatment of hypertensive cardiac remodeling.

Antihypertensive Agents↗
PubMed1995

Systolic ventricular dysfunction and heart failure due to coronary microangiopathy in hypertensive heart disease.

Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.

Antihypertensive Agents↗
PubMed1995

[Cyclosporin in severe steroid-requiring bronchial asthma].

BASIC PROBLEM: Treatment of chronic severe bronchial asthma with corticosteroids is inadequate in a minority of patients and is often accompanied by considerable side effects. Additional specific immunosuppression appears to be therapeutically promising. PATIENTS AND TREATMENT: Three patients (2 women, aged 44 and 29, a man aged 57 years), all with chronic severe asthma requiring corticosteroids, were given cyclosporin (mean dose 1.8 mg/kg; serum level 72 +/- 35 ng/ml) additional to conventional bronchospasmolytic drugs for 9 to 20 months. COURSE: The frequency and intensity of asthmatic attacks markedly decreased in all three patients. The mean peak-flow measurements in the mornings before broncholysis had increased by 23% over the precyclosporin level of the calculated normal value. Peak flow variability improved by 13%. The mean one-second forced expiratory volume (FEV1) rose from 37 to 66% of the normal value (P < or = 0.05) and correlated with the serum cyclosporin level (correlation coefficient 0.58-0.97). The frequency of acute severe asthmatic attacks (FEV1 < or = 40%) requiring additional hospitalization with intravenous administration of glucocorticoids fell by 30%. The systemic corticosteroid maintenance dosage could be significantly reduced or the drug discontinued in two patients. CONCLUSION: These observations indicate that cyclosporin can be useful in the treatment of selected cases of chronic severe steroid-refractory asthma. Prospective studies are needed to judge its long-term efficacy.

Adult↗
PubMed1995

[Recurrent immune thrombocytopenia: a rare complication after contrast medium injection].

HISTORY AND CLINICAL FINDINGS: In a 66-year-old woman with unstable angina, treated with 20,000 IU heparin daily for 6 days, platelet count fell dramatically from 310,000 to 1000/microliters 8 hours after injection of 90 ml of contrast medium (Iopromide) during coronary angiography. In addition to a marked tendency towards spontaneous bleeding she developed a large haematoma at the site of the arterial puncture, with a fall in haemoglobin to 9 g/dl, and acute renal failure. TREATMENT AND COURSE: Red blood cell and platelet infusions were given, together with cortisone, 1000 mg, and immunoglobulins. Platelet count returned to within normal limits after 8 days. Two haemodialyses initiated polyuria, followed by rapid normalization of kidney function. No antibodies against iopromide, iopamidol, heparin or heparinoids were found. At an emergency coronary balloon angioplasty 3 weeks later iopamidol was injected (45 ml). Again there was a profound fall in platelets to 1000/microliters, associated with acute renal failure. Treatment identical to that after the first episode brought about complete normalization. CONCLUSION: The reported reactions were most likely due to immune thrombocytopenia after administration of contrast medium.

Acute Kidney Injury↗
PubMed1995

[Repeated ingestion with suicidal intent of potentially lethal amounts of thallium].

30 minutes after drinking half a cup of rat poison a 16-year-old girl was admitted to hospital. In addition to various enteric detoxification measures forced dialysis was instituted and, after the urinary thallium level had become known (9 mg/l), haemodialysis was begun and ferric ferrocyanide (Prussian blue) administered (0.5 mg daily for six days). She had no symptoms at any time. After 10 days she was discharged. Five days after discharge she was again admitted, with colic-like abdominal pain, vomiting, paraesthesias of the hands and feet, and in a state of agitation. She had once again ingested rat poison, about one cup. Physical examination revealed little of consequence, except diffuse alopecia. Urinary thallium concentration was 37 mg/l. In the electrocardiogram the P-R interval was shortened to 0.11 s and T waves inverted in leads III and V1. Electronmicroscopy of cardiac and skeletal biopsies revealed lipid droplets, increased sarcoplasm and widening of some of the tubules. Treatment consisted of haemodialysis, forced diuresis (1 l urine/h), administration of ferric ferrocyanide, orthograde intestinal infusions and potassium substitution (serum level: 5 mmol/l). After 28 days the patient was discharged into psychiatric care.

Adolescent↗
PubMed1995

[Protection and "preconditioning" of the human heart during percutaneous transluminal coronary angioplasty (PTCA) by intracoronary dipyridamole administration].

BACKGROUND AND AIM: A brief episode of ischemia followed by reperfusion termed "ischemic preconditioning" has been identified as a mechanism rendering the myocardium more resistant to ischemia. Recently adenosine has been identified as an important mediator of ischemic preconditioning. Dipyridamole represents an important drug interfering with myocardial adenosine metabolism by inhibiting its degradation. The aim of this study was to investigate the effect of an intracoronary dipyridamole infusion on the extent and tolerance of myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). PATIENTS AND METHODS: In the first study group 46 patients undergoing coronary angioplasty were randomised to receive dipyridamole or conventional treatment before PTCA. In the second study group 11 patients were investigated, receiving PTCA of restenosis following PTCA carried out 6 months earlier. RESULTS: In the first group as a striking result patients receiving pretreatment with dipyridamole tolerated longer times of balloon inflations (155.3 +/- 68.9 vs. 93.1 +/- 24.7 s), expressed lower severity of cardiac pain, demonstrated less pronounced ST-segment shifts on the surface ECG and showed a lower incidence of arrhythmias. In the second group the first dilatation had been performed conventionally, while pretreatment with dipyridamole had been performed prior to the dilatation of restenosis. Similar to the findings in the first patient group pretreatment with dipyridamole resulted in enhancement of balloon inflation times, regression in cardiac pain and lower extent of ST-segment shift and incidence of arrhythmias. In both study groups intracoronary application of dipyridamole showed no significant impact on heart rate and arterial blood pressure. CONCLUSION: Summarising our results indicate, that intracoronary application of dipyridamole renders the heart more resistant to ischemia.

Aged↗
PubMed1995

Role of nitric oxide in the regulation of coronary vascular tone in hearts from hypertensive rats. Maintenance of nitric oxide-forming capacity and increased basal production of nitric oxide.

In arterial hypertension, coronary flow reserve, expressed by the difference between autoregulated and maximal coronary flow, is frequently impaired. Previous experimental and clinical investigations using acetylcholine as a stimulus for the production of endothelium-derived relaxing factor suggested that an impaired endothelium-dependent vasodilation, presumably caused by a decreased formation of nitric oxide (NO), may account for this microvascular dysfunction. However, so far no study has been performed that quantifies the formation of NO within the coronary circulation of hypertensive hearts to assess its role in setting coronary vascular tone in the hypertensive heart. We therefore quantified NO formation within the coronary circulation of constant flow-perfused, isolated hearts from spontaneously hypertensive rats (SHR, 16th to 26th week), as a model for hypertensive heart disease, and from the normotensive control strain (Wistar-Kyoto, WKY) using the oxyhemoglobin technique. Coronary perfusion pressure and vascular resistance were almost 30% higher in SHR compared with WKY hearts. Intracoronarily applied NO decreased coronary vascular resistance by maximally 45% of resting values in a concentration-dependent manner in both groups. The bradykinin-induced decrease in coronary vascular resistance and the parallel increase in NO release were comparable in SHR and WKY hearts and fell within the vasodilator range of exogenously applied NO. Moreover, basal release of NO normalized to heart wet weight was 50% higher in SHR compared with WKY hearts. Rates of basal NO release were correlated inversely with changes in coronary perfusion pressure and vascular resistance in both groups (r = -.85 and -.84, respectively, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Evaluation of cardiac damage in hypertension.

Functional and structural alterations of the coronary microcirculation and left ventricular hypertrophy represent the two key cardiac manifestations of arterial hypertension. In addition, qualitative changes in myocardial tissue composition and structure, such as reactive interstitial fibrosis, are frequently present. The extent of the impairment of coronary flow reserve can be measured using Doppler, argon gas chromatography or thermodilution techniques. Impaired flow reserve can be detected non-invasively using positron emission tomography. The combination of both a normal coronary angiogram and a positive exercise tolerance test (electrocardiogram or thallium) strongly indicates the presence of a hypertension-related disorder of the coronary microcirculation. Left ventricular hypertrophy can easily be quantified using echocardiography (Penn formula). Diastolic function can be assessed by measuring mitral inflow using pulsed-wave Doppler echocardiography (E/A ratio). Non-invasive assessment of myocardial structural alternations may be possible in the future using backscatter echocardiography.

Coronary Circulation↗
PubMed1995

[Myocardial lactate extraction during programmed ventricular stimulation and its value for etiologically-related therapy of ischemic ventricular tachyarrhythmia].

UNLABELLED: Ischemia is considered to be one of the most important trigger mechanisms of ventricular tachyarrhythmias, i.e., tachycardia (VT) and fibrillation (VF) in coronary artery disease (CAD). The aim of the study was 1) to investigate the relationship between ischemia and inducibility of VT/VF, and 2) to address the question, if removal of ischemia leads to suppression, resp. noninducibility of arrhythmias. In 30 patients (pts) with CAD (healed myocardial infarction in 73%, acute myocardial infarction excluded) and sustained malignant ventricular arrhythmias (VF in 47%, VT in 37%, and arrhythmogenic syncope in 16%) the myocardial lactate extraction (MLE) was calculated by measuring the arterio venous coronary lactate difference simultaneously during programmed ventricular stimulation. Eighteen pts (group A, "lactate-positive") showed a significant decrease of MLE from +16 +/- 13% at rest to -18 +/- 24% during stimulation just before induction of VT/VF (p < 0.0005). During recovery up to 10 min following termination of VT/VF MLE returned to normal range (+19 +/- 16%). In 12 pts (group B, "lactate-negative") MLE showed no significant change between rest, stimulation, and recovery. Compared to group B pts, group A pts demonstrated a significantly higher number and degree of coronary lesions as well as regions with reversible ischemia during 201Tl- scintigraphy. Lactate-positive pts presented spontaneous arrhythmias of higher frequency and had usually a two- or three-vessel disease, while lactate-negative pts presented arrhythmias of lower frequency and had more often a one-vessel disease with ventricular aneurysm. 17/18 (94%) group A pts underwent coronary bypass grafting (11) or balloon angioplasty (6) and were rendered noninducible during post interventional PVS in 94%, showing also a normalized MLE in 87% of cases. In group B only 4/12 pts were suitable for revascularization and could be rendered noninducible in only 50% of cases. With respect to the success-rate of the anti-ischemic therapy in terms of arrhythmia suppression, a lactate-positive result during primary PVS had a sensitivity of 89%, a specificity of 75%, a positive predictive value of 94%, and a negative predictive value of 60%. IN CONCLUSION: in about 60% of pts with VT/VF and significant CAD a correlation between ischemia and inducibility could be demonstrated. MLE during PVS has a highly significant predictive value for the effect of an antiischemic intervention on arrhythmia induction.

Aged↗
PubMed1995

[Autoantibodies against cardiac myosin in patients with myocarditis and dilated cardiomyopathy].

Evidence accumulated in recent years indicates that autoimmunologic mechanisms may play an important role in the pathogenesis of myocarditis and dilated cardiomyopathy. In animal studies with Coxsackie B3-virus-induced murine myocarditis circulating autoantibodies against cardiac myosin have been detected. The present study investigates whether in patients with myocarditis and dilated cardiomyopathy antimyosin-autoantibodies can be detected. Patients with other cardiac diseases and healthy blood donors were used as controls. In 30 of 62 (48.4%) patients with myocarditis antimyosin-antibodies could be detected, whereas in patients with dilated cardiomyopathy only 10 of 41 (24.4%) sera contained antimyosin-antibodies (p < 0.05). In patients with other cardiac diseases, 9 of 43 (21%) sera showed antimyosin-autoantibodies (p < 0.05 vs myocarditis, not significant vs DCM). In healthy blood donors, antimyosin-autoantibodies could only be detected in 1 of 39 (2.5%) sera. In Western-blot tests, the antimyosin-antibodies in patients with myocarditis bound to the myosin heavy chain. Protein A-Sepharose chromatography showed that the antimyosin-autoantibodies are of the IgG-type. No organ-specificity of the antibodies for cardiac myosin could be detected, and the antimyosin-autoantibodies bind equally to myosin prepared from either cardiac or skeletal muscle, respectively.

Autoantibodies↗
PubMed1994

Identification of serotype-specific and nonserotype-specific B-cell epitopes of coxsackie B virus using synthetic peptides.

Coxsackie B viruses are thought to be involved in the induction of myocarditis. However, the diagnosis of acute infections by serology even today is practically impossible. The major problem is that no antigenic determinants of coxsackie B viruses have been identified or characterized which could be used as antigens in a rapid routine antibody screening test. Therefore, we synthesized overlapping peptides according to the sequence of the capsid protein VP1 of coxsackie B3 (CB3) virus in order to identify antigenic determinants located on VP1. Using sera raised against CB3 in mice, we were able to identify several antigenic determinants of CB3. Here we present a characterization of three epitopes found. We also tested the type-specificity of these antigenic determinants by using rabbit antisera against coxsackie viruses B1-B6. One antigenic determinant, peptide VP1-1, representing residues 1-15 of VP1, reacted highly type-specific for CB3. A second antigenic determinant (peptide VP1-3, residues 21-35 of VP1) reacted as well with the anti-CB3 sera as with the anti-CB4 sera. Therefore, the peptide VP1-3 seems to represent a non-type-specific antigenic determinant of coxsackie B viruses. Peptide VP1-24 (residues 229-243 of VP1) showed broad cross-reaction with anti-CB sera except with the anti-CB1 sera. This identification of type-specific and non-type-specific epitopes of coxsackie B viruses may provide the basis for the establishment of an effective and fast antibody screening test for coxsackie B viruses in patients with clinically suspected myocarditis.

Amino Acid Sequence↗
PubMed1994

Therapy of hypertensive cardiac hypertrophy and impaired coronary microcirculation.

In arterial hypertension, cardiac remodeling comprises myocyte hypertrophy, interstitial fibrosis, and functional and structural alterations of the coronary microcirculation. This leads to diastolic and systolic dysfunction of the left ventricle and impairment of coronary flow reserve. Consequently, antihypertensive treatment should aim at repairing hypertensive cardiac remodeling through reversing myocyte hypertrophy, restoring myocardial structure, and improving coronary flow reserve along with blood pressure normalization. Although it has been shown that regression of left ventricular hypertrophy (LVH) can be achieved by suitable antihypertensive therapy, more insight regarding the ability to repair coronary microcirculation is needed. In spontaneously hypertensive rats (SHRs), it has been shown that coronary reserve was enhanced after hydralazine administration without concomitant regression of LVH. Likewise, administration of the calcium-channel blocker felodipine led to a reversal of medial hypertrophy in coronary resistance vessels. The angiotensin-converting enzyme inhibitor lisinopril was shown to improve coronary reserve and to reserve both medial hypertrophy and myocardial fibrosis in SHRs. Increase in length density of capillaries with either nifedipine or moxonidine treatment was also found in experimental hypertension. First clinical data indicate that, after prolonged antihypertensive treatment, coronary flow reserve can be improved in hypertensive patients with microvascular disease. Further studies are warranted to elucidate whether improved coronary flow reserve after medical treatment for arterial hypertension is due to an influence of myocardial factors, such as LVH or myocardial fibrosis or to repair of the structurally remodeled microcirculation.

Animals↗