Johann Dusleag

Effects of benazepril and metoprolol OROS alone and in combination on myocardial ischemia in patients with chronic stable angina.

The efficacy of benazepril, metoprolol OROS and their combination was evaluated in 29 patients (42 to 74 years of age) with chronic stable angina and documented coronary artery disease in a placebo-controlled, double-blind, crossover trial using serial quantitated exercise testing and ambulatory electrocardiographic (ECG) monitoring. The mean (+/- SEM) exercise time was 8.5 +/- 0.7 min with placebo, 8.3 +/- 0.6 min (95% confidence interval [CI]-1.06 to 0.54) with benazepril, 9.4 +/- 0.5 min (95% CI -0.32 to 2.14) with metoprolol OROS and 9.6 +/- 0.5 min (95% CI -0.25 to 2.47) with the combination of benazepril and metoprolol OROS. The mean exercise time to the development of 1 mm ST segment depression was prolonged from 6.0 +/- 0.6 min with placebo to 6.3 +/- 0.6 min (95% CI -0.93 to 1.45) with benazepril, 7.9 +/- 0.5 min (95% CI 0.83 to 3.0) with metoprolol OROS and 8.1 +/- 0.6 min (95% CI 0.88 to 3.29) with the combination of benazepril and metoprolol OROS. Benazepril did not alter the rest or maximal heart rate, whereas metoprolol OROS alone and in combination significantly lowered the heart rate at rest and during maximal exercise. Systolic blood pressure at rest was nonsignificantly reduced, whereas diastolic blood pressure was lowered significantly by all treatments in comparison with placebo. At maximal exercise, only metoprolol OROS, whether given alone or in combination with benazepril, was able to blunt significantly systolic blood pressure and rate-pressure product.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term outcome and prognostic factors in dilated cardiomyopathy : preliminary results

To investigate long-term follow-up and identify prognostic factors in patients with dilated cardiomyopathy (DCM) the authors investigated 167 consecutive patients on an outpatient basis. All patients underwent left- and right-heart catheterization; follow-up comprised clinical and echocardiographic investigations. Results: After a mean follow-up period of ninety-three ± thirty-six months 82 patients (49%; 71 men, 11 women, mean age fifty-five ± eleven years) were alive. 29 of them (27 men, 2 women, mean age fifty-two ± nine) showed normal left ventricular ejection fraction (LVEF) after a mean follow-up period of one hundred four ± forty months. The remaining 53 patients (44 men, 9 women, mean age fifty-six ± eleven) revealed LVEF similar to that of the first examination. Eighty-five patients died (51%; 73 men, 12 women). Causes of death were the following: progressive heart failure, 24; sudden death, 23; stroke, 3; pulmonary embolism, 2; noncardiac death, 4; unknown causes, 29. The median period from the onset of first symptoms until definite diagnosis was two months in patients with stable conditions, three months in those with normalization of LVEF and twenty-four months in those who died, respectively (P < 0.01). At the time of diagnosis, patients with stable outcome had a mean LVEF (LVEF 1) of 37%, those who returned to normal had 40% (ns). Patients who died had a mean LVEF 1 of 32% and therefore differed significantly from both groups of survivors (P < 0.001). Left ventricular enddiastolic pressure (LVEDP) at the time of diagnosis was highest in patients who died (22 mmHg) and therefore differed significantly from both groups of survivors (normalization: 16 mmHg, stable patients: 18 mmHg, P < 0.001). Conclusions: According to their results, time until diagnosis, LVEF, and LVEDP are prognostic indicators. No difference was noted between the groups concerning etiology, medical treatment, or functional classification according to the New York Heart Association.

Current views on mechanisms of vasodilation in response to ischemia and hypoxia

Myocardial function (and thus life) is entirely dependent on sufficient O2 supply. Therefore, this supply is extremely well regulated via a refined system of interacting mechanisms. These have been subject to extensive research for more than 100 years. Surprisingly, remarkable dispute still arises among scientists concerning the factors and mechanisms involved in this regulatory system.During ischemia, myocardial cells have been shown to release vasoactive metabolites (eg, H+ and K+ ions, lactic acid, adenosine, and others), which cause spontaneous coronary dilation. On the other hand claims have been made that the endothelium itself could play a key role in hypoxic/ischemic vasodilation by releasing endothelium-derived relaxant factor (EDRF) (NO = nitric oxide) and other still partially unspecified vasoactive substances (eg, prostaglandins). Furthermore, it has been discussed that intravascular O2 tension (pO2) itself would exert a direct effect upon endothelial and/or vascular smooth muscle cells and thus produce per se a local reflectory vasodilation. In contrast, the intravascular CO2 tension has also been shown to act upon coronary vascular resistance during myocardial ischemia. Recently, hints have been made about the membrane potential of arterial smooth muscle cells as a key factor in hypoxia/ischemia vasodilation. However, during hypoxia and metabolic inhibition, the membrane potential seems to be modulated primarily by the action of adenosinetriphosphate-dependent (ATP) potassium channels (KATP+ channels).In conclusion, a number of factors contribute to ischemia/hypoxia-induced vasodilation. The present review contrasts recent findings on ATP-dependent K+ channels with other experimental evidence concerning other mechanisms involved in hypoxic/ischemic vasodilation.

Circadian Blood Pressure Pattern in Patients with Treated Hypertension and Left Ventricular Hypertrophy

Left ventricular hypertrophy in hypertensives is an important determinant of prognosis. In the present study 45 patients with treated essential hypertension were divided into two groups: 23 patients had normal left ventricular dimension and 22 patients had echocardiographic signs of left ventricular hypertrophy (LVH). All patients were adequately treated during daytime, but ambulatory blood pressure monitoring showed a distinct abnormal pattern in the LVH group characterized by a lack of blood pressure reduction during the night; 16 of 22 patients with LVH had no blood pressure decline during the night, whereas 17 of 23 patients without hypertrophy showed this reduction (P < 0.01). In conclusion, patients with hypertension and LVH often reveal a lack of blood pressure decline during the night, which may be the reason for the development of left ventricular hypertrophy (and thus should be managed by a different circadian blood pressure therapy) or which may be the consequence of progressive structural changes in the resistance vessels, along with the development of left ventricular hypertrophy. It is suggested that patients with hypertension and left ventricular hypertrophy should have ambulatory twenty-four hour blood pressure monitoring.

Frequency of magnetic resonance signal abnormalities of the brain in patients aged <50 years with idiopathic dilated cardiomyopathy

Twenty patients with idiopathic dilated cardiomyopathy (IDC) aged <50 years (mean 41) and an age-matched group of 20 healthy volunteers were studied. All subjects were free of cerebrovascular symptoms and risk factors for stroke. Magnetic resonance imaging of the brain, extracranial Doppler ultrasonography, heart catheterization and echocardiography were performed. In patients with IDC, a higher frequency of ventricular enlargement (p < 0.02), cortical atrophy (p < 0.01) and white matter lesions (p <0.05) was observed. Cerebral infarcts were found in 4 patients (p < 0.05) who showed clinically severe limitation of functional capacity (New York Heart Association class III or IV). The extent of cortical atrophy, and the duration of clinical evidence of IDC showed a significant correlation (p < 0.04). The data indicate a high incidence of parenchymal abnormalities of the brain in young, neurologically asymptomatic patients with IDC.

Reversibility of dilated cardiomyopathy by low-dose oral roxithromycin in a patient with chronic lyme-borreliosis

It has been shown earlier that dilated cardiomyopathy can be associated withBorrelia burgdorferi infection.Here the authors present a case: a fifty-nine-year-old man who presented with dyspnea, oligoarthritis, paresthesia in both hands, and acrodermatitis chronica atrophicans. Upon further cardiologic exploration by cardiac catheterization and two-dimensional echocardiography (volume-length-area method), the patient exhibited an ejection fraction (EF) of 49%. Serology revealed IgG ELISA positive and IIFT 1:64 positive forB. burgdorferi. The patient received 2 × 150 mg roxithromycin orally for six weeks. Upon a second examination after termination of treatment (three months later), the patient presented with negativeB. burgdorferi serology and normal EF (70%). While cardiac manifestations thus apparently vanished, other symptoms persisted.This case may give new insight into mechanisms of action of macrolides againstB. burgdorferi (a field where information is inherently scant). One may, however, argue that in a well-perfused organ like the heart, tissue-activity of roxithromycin may suffice in order to unfold its activity againstB. burgdorferi.

A Most Unusual Case of a Whole Family Suffering from Late Lyme Borreliosis for Over 20 Years

trian family (Bb is endemic in the area of Graz, Austria) who have suffered from Lyme disease for a period of more than twenty years. The wife is forty-three years of age and acquired Bb in 1968 with a most typical history of tick bite, erythema chronicum migrans, flu-like symptoms (stage I), and subsequent classical symptoms of Bb-associated disorders (arthritis, cranial neuritis, meningitis, and later, chronic arthritis, chronic radiculitis, depression-stages II and III). Her husband, fifty years of age, had no memory of a primary infection with classical stage I symptoms but remembers recurrent episodes of flu-like symptoms a year after the infection of his wife. These episodes were soon followed by stage II and III symptoms. Later he was treated several times for ventricular arrhythmias (Lown VIb), whereupon electrophysiological stimulation of the His bundle was performed. A son was born in 1969, who, at his birth, suffered from several minor abnormalities like a

Observations on Plasma ANP Levels During Short-Term Transient Myocardial Ischemia Produced by PTCA in Patients with LAD Stenosis

Ten patients with coronary artery disease and stable angina (mean age fifty- seven) were included in the study. Five of the patients had normal left ventricu lar function, 5 had local hypokinesia or akinesia; 8 had one-stem and 2 had two- stem disease, but all had left anterior descending (LAD) lesions ranging from 75% to 100%. Ejection fraction varied between 35% and 75% (mean 59%). Im munoreactive atrial natriuretic polypeptide (ANP) levels in the femoral vein (FV) and the coronary sinus (CS) were measured before, immediately after, and up to twenty-four hours after percutaneous transluminal coronary angioplasty (PTCA) of the LAD. ANP secretion increased by 83% (FV) and 11% (CS) with in minutes after PTCA and reached control levels after thirty to sixty minutes. In patients with hypokinesia of the anterior wall, ANP secretion was significantly lower, 48% (FV) and 11% (CS) respectively. ANP secretion during PTCA was higher in patients with concomitant increase in pulmonary capillary pressure (PCP) but was also observed without an increase of PCP, suggesting ventricular ANP secretion. In conclusion, transient myocardial ischemia leads to immediate ANP secre tion even in the absence of significant pressure elevation in the left atrium. As a part of the continuous medical education program of the American Col lege of Angiology the second part of the paper reviews the mechanisms that al low the ischemic heart to counteract the ischemic condition and thus to escape from myocardial infarction. A review on this subject is presently not available in the literature.