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Biomedical subjects

M Vogt

Publications and source records attributed to M Vogt.

At least 109 records · Page 6Linked to original sources
PubMed1994

[Long-term antihypertensive therapy with isradipine. Improvement of coronary flow reserve in patients with arterial hypertension and microvascular angina].

Antihypertensive Long-term Therapy with Isradipine/Improvement of coronary flow reserve in patients with arterial and microvascular angina In patients with arterial hypertension coronary flow reserve is often impaired due to left ventricular (LV) hypertrophy and alterations of the coronary microcirculation. Experimental and clinical studies have shown that calcium channel blockers can induce regression of myocardial hypertrophy. Objective of the present study was to see whether chronic antihypertensive treatment with calcium channel blockers can improve the diminished coronary reserve in patients with arterial hypertension and microvascular angina pectoris. Fifteen hypertensive patients with microvascular angina (61 +/- 7 years, normal coronary angiogram, mild LV-hypertrophy) were treated with isradipine (CAS 75695-93-1) (5.3 +/- 0.9 mg/d) for 12 +/- 2 months. Before and after therapy (after a washout period of 1 week) coronary flow was quantitatively measured by the gas chromatographic Argon method. Coronary reserve was calculated as the quotient of coronary resistance under baseline conditions and after dipyridamole (0.5 mg/kg i.v.). Under isradipine therapy systolic blood pressure was lowered from 165 +/- 20 to 140 +/- 13 mmHg (p < 0.01) and diastolic blood pressure from 98 +/- 8 to 88 +/- 6 mmHg (p < 0.01). The LV muscle mass index decreased by 10% from 154 +/- 33 to 139 +/- 28 g/m2 (p < 0.05). Baseline coronary blood flow (81 +/- 13 versus 83 +/- 16 ml/min x 100 g, n.s.) was identical before and after therapy. There were also no differences in coronary perfusion pressure, heart rate, myocardial oxygen consumption and arterio-coronary venous oxygen difference before and after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Tetanic equivalents, cephalgia, absences].

Real hypoparathyroidism may develop after surgery of the thyroid, more rarely of the parathyroid. The idiopathic form is thought to be connected with autoimmune processes. We present the case of a female patient with acquired hypoparathyroidism after strumectomy 40 years ago. A clinical picture, not only with neurologic and dermatologic manifestations but also late organic sequelae of chronic hypocalcemia, i.e. calcification of basal ganglia, had developed impressively. Without the proof of laboratory tests diagnosis is difficult to establish at the first go in medical practice, since clinical symptoms may be few or widely scattered. Since the rate of strumectomies has dropped as a consequence of restricted indications, acquired hypoparathyroidism has become rarer. A simple long-term treatment with vitamin D and calcium relieves the patient from tetanic problems and prevents severe and irreversible late organic lesions.

Aged↗
PubMed1993

[The prognostic value of different patterns of change in the CD4 lymphocyte counts in 420 symptom-free HIV-1-infected persons].

The pattern of change over time of CD4-lymphocyte counts was investigated prospectively in 420 patients infected with HIV-1 (106 women, 314 men; mean age 34.9 [21-70] years) to assess its value in prognosticating progression to AIDS. Only those CD4-lymphocyte values were taken into account which had been measured in the asymptomatic stage of the HIV infection and before introduction of antiviral treatment. An average of 4.5 (range 3-10) measurements per person were available. Mean observation time was 2.4 years, the mean annual CD4-lymphocyte decrease was 48 cells/microliters. 121 patients (28.8%) had a fall in CD4-lymphocyte count which in the regression analysis significantly differed from zero. In this group there occurred 19 progressions to AIDS (15.7%), in contrast to only 20 (6.6%) in the 299 patients with a nonsignificant CD4 fall (P < 0.01). Multivariate analysis with the Cox regression indicated that the annual reduction in the CD4 count and the initial CD4 count were the only values of prognostic significance regarding progression to AIDS. There was no evidence that percentage and absolute CD4-lymphocyte counts had a different predictive value. When the initial CD4 count was high (> 900 cells/microliters), there was on average a steeper reduction in CD4-lymphocyte counts than when it was lower. This findings argues against a linear CD4 fall during the total period of observation. The annual CD4 fall, described with linear regression, is a prognostic criterion on its own for early recognition of those patients at a high risk of progression to AIDS while still in the asymptomatic stage of HIV infection.

Acquired Immunodeficiency Syndrome↗
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

Pathophysiology and clinical aspects of hypertensive hypertrophy.

Individuals with hypertension and electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH) have a 10-fold greater risk of developing cardiac failure than hypertensives without ECG evidence of LVH. LVH in hypertension is characterized by myocardial fibrosis and structural changes to the small intramural arteries. Hypertensives with or without LVH have reduced coronary vasodilator reserve due to hypertensive disease of small coronary arteries. Prognosis of arterial hypertension is largely determined by cardiac complications. The aim of treatment of hypertensive heart disease is to reverse myocardial hypertrophy in order to prevent progression to hypertensive heart failure, as well as reversal of the hypertensive disease of small coronary arteries in order to improve coronary reserve. On the development of hypertensive heart failure, administration of digitalis, diuretics and angiotensin converting enzyme (ACE) inhibitors should be initiated. Although regression of LVH can be induced by dihydropyridine calcium channel blockers, ACE inhibitors and sympatholytic substances, clinical evidence of the reversal of hypertensive disease of small coronary arteries has still to be established.

Adrenergic beta-Antagonists↗
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

[Functional results of patellectomy].

A follow-up of 41 patients 1-10 years after patellectomy was performed. A discrepancy between subjective satisfaction of the patient and objective functional results could be observed. Best results can be expected after patellectomy due to traumatic comminution of the patella. Patellectomy due to degenerative destruction of the patella results in decreasing pain but exercises only low influence on the functional result. Instability after patellectomy can be explained by loss of the major patellar function (sesamy bone in the patella and quadriceps tendon). The intact patella is of great importance. However, patellectomy of destroyed patellas is considered very helpful. Competent concomitant and after treatment as well as an accurate diagnosis at the right time are prerequisites for good results.

Adolescent↗
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

[Rhabdomyolysis in body building. Report of a case and literature review].

A 24-year-old man was sent to the emergency unit and evaluated with the symptom of acute right-sided chest pain. Myocardial infarction and pulmonary embolism were excluded. A creatine kinase (CK) serum concentration of 17,034 U/l (normally up to 270) was found. The patient gave a history of excessive body-building exercises on the previous day. During the follow-up period symptoms resolved within several days, and CK values gradually diminished. A review of current literature on rhabdomyolysis in patients with body-building is presented.

Adult↗
PubMed1992

[Embolizing aortic valve endocarditis in the differential diagnosis of thrombotic thrombocytopenic purpura].

A 50-year-old man complained of lumbar pains, lack of energy, dysarthria and ataxic gait. Investigation revealed progressive anaemia (haemoglobin initially 10.5 g/dl, later 6.8 g/dl) and thrombocytopenia (initially 67,000/microliters, later 25,000/microliters). In addition he had unexplained pyrexia of up to 39.8 degrees C. Lactate dehydrogenase was 780 U/l and fragmented red cells were noted in the blood film. Because of suspicion of thrombotic thrombocytopenic purpura, treatment with fresh plasma by infusion was immediately initiated. On the third day of treatment he developed left ventricular failure; auscultation revealed a blowing early diastolic murmur over Erb's point together with a spindle-shaped early diastolic murmur over the right second intercostal space. Computed tomography of the skull showed recent haemorrhage into the left half of the cerebellum and an older right posterior infarct. The abdominal ultrasound scan suggested a haemorrhagic spleen infarct. In view of these findings the diagnosis was revised to embolizing aortic endocarditis with aortic reflux (confirmed by colour Doppler echo-cardiography). Aortic valve replacement was performed immediately, and the patient was treated with gentamycin 80 mg/d and teicoplanin 400 mg/d for four weeks. Postoperatively he was given 12 units of platelet concentrate and the platelet count remained stable thereafter (greater than 100,000/microliters). Splenectomy became necessary because the splenic haematoma increased in size during oral anticoagulant therapy. After a 6 week hospital stay the patient was discharged in good condition.

Anti-Bacterial Agents↗
PubMed1992

[Antiviral drug therapy of infections caused by Herpes simplex and Varicella Zoster viruses].

Herpes simplex virus type 1 and 2 may cause painful mucocutaneous lesions in both immunosuppressed and immunocompetent patients. Indications for the use of acyclovir (ACV) are reviewed. In the second part the management of infections caused by varicella-zoster virus are discussed. Primary varicella (chickenpox) in immunosuppressed children should be treated with i.v. ACV without delay. In healthy patients varicella pneumonia needs to be treated with ACV. Healthy patients with herpes zoster are not usually candidates for antiviral therapy. The only exception is herpes zoster ophthalmicus. In patients with severe immunosuppression, such as transplant recipients, ACV therapy is recommended in order to reduce the rate of dissemination. First reports and our own observations on the development of ACV-resistant HSV and VZV isolates stress the importance of discriminating use of ACV and other antiviral compounds in immunosuppressed patients.

Acyclovir↗
PubMed1992

[Pericardectomy and acute infectious pericarditis].

Between 1980 and 1990 12 patients (5 male, 7 female) were operated on for acute infectious pericarditis at a mean age of 42 years. The infections were 6 bacterial (purulent 4, abscess 2), 4 tuberculous, 1 viral and 1 Candida. Pericarditis resulted from contiguous spread of infection from bilateral pneumonia in 3 patients, from subphrenic abscess in 2 and followed bacteremia in 1. Clinical signs were: tamponade/shock in 9, elevated jugular venous pressure in 11, edema in 6, hepatomegaly in 6, ascites in 1, and pericardial friction rub in 3. A preoperative pericardiocentesis in 9 patients allowed only 4 positive microbiological diagnoses and was an insufficient drainage in all cases. The preoperative mean NYHA class was 3.3. The pericardectomy was total in 9 patients and partial in 3. Total mortality was 1/12 patients (8%) with one late death due to recurrent tuberculous pericarditis. No patient with purulent pericarditis died. Another recurrence occurred 6 months after acute viral pericarditis. Atrial fibrillation in one patient was the only postoperative complication. After a mean follow-up period of 48.5 months no cardiac constriction had occurred in 11 surviving patients Actuarial survival after pericardectomy is 100% after 1 month and remains 91% after 5 years. The mean NYHA class has significantly improved to 1.2 (p less than 0.05) at the end of the follow-up. We conclude that pericardectomy combined with a specific antimicrobial therapy is a safe treatment for acute infectious and especially purulent pericarditis with low mortality and excellent longterm results. Early pericardectomy allows rapid decompression of the heart, removal of intrapericardial adhesions and infected tissue and prevents late constriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗