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Biomedical subjects

B Maisch

Publications and source records attributed to B Maisch.

At least 163 records · Page 9Linked to original sources
PubMed1996

Drug withdrawal and rebound hypertension: differential action of the central antihypertensive drugs moxonidine and clonidine.

To examine the antihypertensive action of the centrally acting antiadrenergic drugs moxonidine and clonidine, systolic and diastolic blood pressure as well as heart rate were monitored by radio telemetry in spontaneously hypertensive rats (SHR) with established high blood pressure. Increasing doses were administered with regular rat chow for 6-8 day periods. Moxonidine reduced (p < 0.05) diastolic blood pressure at a dose of 8 mg/kg/day and systolic blood pressure at 13 mg/kg/day. Heart rate was reduced during high activity of rats corresponding to an antitachycardiac action. After withdrawal of 18 mg/kg administered for only 1 day, blood pressure returned to pretreatment values within 8 days. Clonidine reduced systolic and diastolic blood pressure at 0.3 mg/kg/day. At 0.8 and 1.3 mg/kg/day, systolic blood pressure reduction was less pronounced, although heart rate was reduced further, reaching values that were below those of untreated sleeping rats. When 1.3 mg/kg/day clonidine was discontinued, systolic as well as diastolic blood pressure increased above pretreatment values within 1 day. A rebound was also observed in heart rate, which increased by 150 beats/ min. A comparable rebound in blood pressure was observed after withdrawal of 0.3 mg/kg/day. Since a blood pressure rebound occurred also after withdrawal of 0.3 mg/kg/day clonidine in normotensive rats, the rebound phenomenon was independent of the presence of high blood pressure. No blood pressure rebound was observed when moxonidine (8 mg/kg/ day) was administered (chow or gavage) in normotensive rats. These findings in unanesthetized undisturbed rats demonstrate distinct differences in the mode of action of moxonidine and clonidine, which can be accounted for by specific interactions of moxonidine with imidazoline I1-receptors, whereas clonidine would interact not only with I1-receptors but also with alpha2-adrenoceptors, and most probably also with the vagal activity. In view of our previous studies demonstrating a rise in blood pressure and heart rate after a hypercaloric dietary intake, the selective I1-receptor agonist moxonidine appears particularly appropriate for treating overweight hypertension associated with an enhanced sympathetic outflow of the brain. Of importance in this respect is that a moxonidine-induced reduction in sympathetic outflow was not associated with a gain in body weight but resulted in reduced caloric intake.

Animals↗
PubMed1996

Immunosuppressive and immunomodulatory treatment for myocarditis.

This review examines the immunologic rationale for immunosuppressive and immunomodulating therapy. The controversy as to whether immunosuppressive treatment is beneficial in myocarditis will continue even after the Myocarditis Treatment Trial, which demonstrated that in active myocarditis identified by the Dallas criteria but without taking into account presence or persistence of viral RNA or DNA or signs of autoreactivity, immunosuppression did not influence either central or hemodynamics or prognosis significantly. These findings concur in part with data from experimental mice and also with sporadic human data. In the acute stage of inflammatory viral heart disease, immunosuppressive drugs should be avoided. This recommendation can be upheld even in the light of the Myocarditis Treatment Trial. It is still unresolved, however, whether this also applies in chronic myocarditis with (enteroviral) persistence, in which the residual viral genome may have been rendered noninfective, making it the equivalent of a "scar" or "tombstone" of former infection. Here, demonstration of the viral genome in does not necessarily imply actively replicating virus. Furthermore, evidence is accumulating that the formerly reported incidence of enteroviral persistence in endomyocardial biopsies may have been overestimated. In autoreactive forms of myocarditis with documented humoral and cellular effector mechanisms, studies indicate that immunosuppressive treatment may be useful. However, data from the double-blind, randomized European Study of the Epidemiology and Treatment of Cardiac Inflammatory Disease must be awaited before conclusions can be made. We therefore recommend enrolling virus-negative patients in randomized, controlled treatment trials to validate the benefit of these treatment regimens. In addition, hyperimmunoglobulin therapy appears to be of particular interest because it has shown few side effects but has positive results in cytomegalovirus-associated myopericarditis in humans.

Adjuvants, Immunologic↗
PubMed1996

Influence of D-net (European GSM-Standard) cellular phones on pacemaker function in 50 patients with permanent pacemakers.

The widespread use of cellular phones in the last years has prompted some recent studies to suggest an interference of pacemaker function by cellular phone usage. To determine the risk of pacemaker patients using D-net cellular phones, we tested 50 patients with permanent pacemakers after routine pacemaker check by short phone calls using a cellular phone (Ericsson, D-net, frequency 890-915 MHz, digital information coding, equivalent to the European Groupe Systemes Mobiles standard). A six-channel surface ECG was continuously recorded from each patient to detect any interactions between pacemakers and cellular phones. Phone calls were repeated during the following pacemaker settings: (1) preexisting setting; (2) minimum ventricular rate of 90 beats/min and preexisting sensitivity; and (3) minimum ventricular rate of 90 beats/min and maximum sensitivity without T wave oversensing. Only 2 (4%) of 50 patients repeatedly showed intermittent pacemaker inhibition during calls with the cellular phone. Both pacemakers had unipolar sensing. Therefore, although interactions between cellular phone use and pacemaker function appear to be rare in our study, pacemaker dependent patients in particular should avoid the use of cellular phones.

Aged↗
PubMed1996

Heart rate variability and major arrhythmic events in patients with idiopathic dilated cardiomyopathy.

This prospective study of 71 patients with idiopathic dilated cardiomyopathy (IDC) and preserved sinus rhythm was designed to evaluate the relation between heart rate variability (HRV) and subsequent major arrhythmic events. Standard time- and frequency-domain HRV parameters were obtained from analysis of 24-hour Holter ECG recordings. During a mean follow-up of 15 +/- 5 months, major arrhythmic events including sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death occurred in 10 of the 71 study patients (14%). Neither time- nor frequency-domain indices of HRV differed significantly between patients with and patients without subsequent major arrhythmic events. However, there was a trend toward a lower standard deviation of the average normal RR interval for all 5-minute segments of the 24-hour recording (68 +/- 17 ms vs 80 +/- 31 ms; P = 0.06) in patients with major arrhythmic events. In addition, the percentage of adjacent normal RR intervals differing > 50 ms over the recording period tended to be lower in patients with major arrhythmic events (6% +/- 3% vs 9% +/- 6%; P = 0.08). Our results indicate a tendency toward attenuated parasympathetic activity in IDC patients with subsequent major arrhythmic events compared to arrhythmia-free patients. Larger studies with longer follow-up periods are necessary to clarify the role of HRV measurements for arrhythmia risk prediction in patients with IDC.

Adolescent↗
PubMed1996

Clinical significance of increased OT dispersion in the 12-lead standard ECG for arrhythmia risk prediction in dilated cardiomyopathy.

QT dispersion was determined from the 12-lead standard ECGs from 107 patients with idiopathic dilated cardiomyopathy (IDG) and compared to QT dispersion measurements in 100 healthy age and sex matched controls. QT dispersion, rate corrected QT dispersion and adjusted QTc dispersion were significantly greater in patients with IDC compared to controls. During a prospective follow-up of 13 +/- 7 months, arrhythmic events, defined as sustained VT, VF, or sudden death, occurred in 12 (11%) of 107 study patients with IDC. QT dispersion was increased in patients with arrhythmic events compared to patients without arrhythmic events during follow-up (76 +/- 17 vs 60 +/- 26 ms; P = 0.03). Differences in QTc dispersion and adjusted QTc dispersion between patients with and without arrhythmic events, however, failed to reach statistical significance. Thus, although QT dispersion was increased in patients with IDC and arrhythmic events during follow-up, its clinical usefulness for risk stratification appears to be very limited due to the large overlap of QT dispersion among patients with and without arrhythmic events.

Arrhythmias, Cardiac↗
PubMed1996

Value of time- and frequency-domain analysis of signal-averaged electrocardiography for arrhythmia risk prediction in idiopathic dilated cardiomyopathy.

Signal-averaged electrocardiography (SAECG) was performed in 120 consecutive patients with idiopathic dilated cardiomyopathy (IDC), and in 60 healthy controls. Time-domain analysis of SAECGs revealed ventricular late potentials in 27 of 120 patients with IDC (23%) compared to 2 of 60 controls (3%; P < 0.05). Frequency-domain analysis of SAECGs showed ventricular late potentials in 9 of 120 patients with IDC (8%) compared to none of the 60 controls (0%, P < 0.05). During a prospective follow-up of 15 +/- 7 months, serious arrhythmic events, defined as sustained ventricular tachyarrhythmias or sudden death, occurred in 17 of 120 patients with IDC (14%). The sensitivity, specificity, and positive and negative predictive values of ventricular late potentials for serious arrhythmic events were 35%, 80%, 22%, and 88% for the time-domain analysis, and 18%, 94%, 33%, and 87% for the frequency-domain analysis of SAECG, respectively. Thus, neither the time-nor the frequency-domain analysis of SAECG appears to be useful for risk stratification in the setting of IDC in view of their low sensitivity and low positive predictive value for serious arrhythmic events during follow-up.

Action Potentials↗
PubMed1996

Ventricular remodeling.

Ventricular remodeling is a repair process. It can follow myocardial infarction, mechanical overload (for example, in hypertension or valvular heart disease), and also occurs in inflammation and dilated cardiomyopathy. Remodeling can be an (early) adaptive process followed by a maladaptive (late) phase and involves all cells that are present in the myocardium - the myocyte, the interstitial cells, the vascular endothelium, and the immune cells. Despite the varying etiopathology that these different aspects of heart disease share, a similar sequence of molecular, biochemical and mechanical events that can lead to heart failure, myocyte hypertrophy, extensive extracellular matrix production and fibrosis, even in patients who were previously unaffected by the original disease process (for example, inflammation or infarction). Heart failure can be influenced by treatment of the underlying disease and by modification of the remodeling process, for example, by ACE inhibitors (cardioreparation). In experimental animals it has been clearly demonstrated that ACE inhibitors may even prevent a genetically predetermined left ventricular hypertrophy (cardioprevention).

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Alcohol and rhythm disturbance: the holiday heart syndrome.

The association between alcohol use and rhythm disturbances, particularly supraventricular tachyarrhythmias in apparently healthy people is called "holiday heart syndrome". The syndrome was first described in persons with heavy alcohol consumption, who typically presented at weekends or after holidays, but it may also occur in patients who usually drink little or no alcohol. The most common rhythm disorder is atrial fibrillation, which usually converts to normal sinus rhythm within 24 hours. The incidence of the holiday heart syndrome depends on the drinking habits of the studied population. The holiday heart syndrome should be considered particularly as a diagnosis in patients without overt heart disease presenting with new onset atrial fibrillation. Though recurrences occur, the clinical course is benign and specific antiarrhythmic therapy is usually not warranted.

Alcohol Drinking↗
PubMed1996

[Alcohol and myocarditis].

The direct toxic effect of alcohol and its metabolite acetaldehyde has been demonstrated both in laboratory animals and in humans. Alterations in the mitochondrial ultrastructure and the dilatation of the sarcoplasmatic reticulum have been shown after an acute infusion of alcohol in the heart. These changes correlate with decreased mitochondrial function, defects in protein synthesis and the occurrence of arrhythmias. The risk of developing alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking, but there is much individual susceptibility to the toxic effect of alcohol. Most patients, in whom alcoholic cardiomyopathy develops, have been drinking over 80 g/d for more than 5 years. The clinical diagnosis of alcoholic cardiomyopathy reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease was found. In studies focussing on alcoholic cardiomyopathy the surprising histologic findings in endomyocardial biopsy in about 30% of all cases was myocarditis with a lymphocytic infiltrate in association with myocyte degeneration or focal necrosis. In myocarditis, the network of microtubules and intermediate filaments is also disrupted by the inflammatory reaction which involves resident cells (myocytes, fibroblasts, endothel cells) and systemic cells (granulocytes, macrophages, monocytes, lymphocytes). Changes in the cardiac cytoskeleton and the extracellular matrix may affect contractile function, since the cytoskeleton organizes the intra- and intercellular architecture. After all, in patients with alcohol abuse and myocarditis the immune functioning appears to be compromised. Several studies suggest that heavy drinking alters both lymphocyte and granulocyte production and function. Alcohol consumption per se might harm the immune system. Furthermore, the myocardial damage due to alcohol consumption could initiate autoreactive mechanisms comparable to those in viral or idiopathic myocarditis. Patients with alcohol abuse and myocarditis have a poor prognosis: signs of biventricular failure including tachycardia, hepatomegaly, and peripheral and lung edema are observed. These symptoms are as nonspecific as are various echocardiographic and electrocardiographic changes such as atrial and ventricular arrhythmias which may be associated both with myocarditis, alcoholic cardiomyopathy and acute effects of drinking without hemodynamic alterations. For the management of patients with alcohol abuse the prevention of further alcohol intake is mandatory to reverse the myocardial damage and the unfavorable predisposition for infection. Specific treatment of myocarditis is the second important option, and treatment of heart failure by reducing the size of the dilated heart and alleviating the signs and symptoms of heart failure is a logical third step.

Acetaldehyde↗
PubMed1996

[Hypertension and alcohol: central and peripheral mechanisms].

Despite intense research efforts, the etiology of primary hypertension remains ill-defined. During our work on molecular influences of lifestyle factors on hypertension, the question arose to what extent cellular and molecular events could be involved in alcohol-induced hypertension. There is increasing evidence that alcohol initiates central as well as peripheral reactions which in a synergistic manner have a hypertensive action. Thus, alcohol diminishes the baro (presso) reflex by interacting with receptors in the brain stem, i.e. nucleus tractus solitarii and rostral ventrolateral medulla. In addition, alcohol induces an increased sympathetic outflow, most probably linked to secretion of corticotropin-releasing hormone. The increased sympathetic outflow is expected not only to induce adrenoceptor-mediated reactions (vasoconstriction, heart rate increase) but to stimulate oxidation reactions. Deleterious peripheral actions result from acetaldehyde which binds to macromolecules if the abundance of cysteine and glutathione is limited. This acetaldehyde induced reduction of low molecular weight thiol compounds can be interpreted as "oxidative stress" which has various unfavourable consequences. The hypertensive action of alcohol should be taken into account when discussing its potential protective influence on coronary risk.

Acetaldehyde↗
PubMed1996

Myocarditis--cardiomyopathy. Consensus Report of the German Association for Internal Medicine, presented at the 100th annual meeting, Wiesbaden, 13 April 1994.

On the basis of several, partially divergent definitions, myocarditis-unlike the often aetiologically unexplained (idiopathic) cardiomyopathies (dilated, hypertrophic, restrictive)-can be classified as c specific disease of the myocardium. This disease often has a known cause and can be due to a large variety of aetiological agents (viral, autoreactive, toxic, infectious processes, etc.) (1). A question still to be answered is whether there is a connection between dilated cardiomyopathy and myocarditis, i.e. whether (virus-induced) myocarditis can progress via a subacute or chronic stage to dilated cardiomyopathy. This question is of considerable diagnostic and therapeutic relevance. The following consensus report thus deals with the clinically important problems related to the diagnosis of myocarditis and dilated cardiomyopathy, examines the aetiological role of immunological mechanisms and discusses the treatment of the two diseases and prognostic factors.

Cardiomyopathy, Dilated↗
PubMed1996

[Indications for transmyocardial laser therapy].

In symptomatic endstage coronary artery disease after full medical therapy (antianginal drugs, betablockers and ACE-inhibitors) further therapeutical options both for the interventional cardiologist with little hope for improvement by PTCA, stent, rotablation and atherectomy and for the cardiac surgeon with bypass surgery and endarterectomy are not available by definition due to the diffuse arteriosclerotic vessel morphology. In those patients one can therefore consider transmyocardial laser therapy (TMR) as the ultimate treatment option. It then is primarily a palliative measure to reduce the patient's symptoms. Improving perfusion and prognosis remains the most important goals, however. TMR can be utilized as the only revascularizing treatment measure or in combination with CABG or PTCA. According to data from international registries, few controlled and several non controlled studies and our own registry in Marburg with now 101 patients improvement of angina and/or dyspnoea can be expected in more than 60% of patients with end stage coronary artery disease (CAD). The patient cohort comprises symptomatic individuals after CABG or multiple PTCAs or with diffuse CAD in diabetes mellitus or with most severe hypercholesterinemia. We consider these above mentioned criteria as the only validated criteria to enter patients with endstage CAD in our controlled study. Hypothetical options for treatment by TMR such as vasculopathies after heart transplantation, cardiomyopathies under the notion of a possible but not proven microangiopathy are not accepted in our institution at present. Before TMR all patients are assessed for their angina class according to the Canadian Cardiac Society (CCS I-IV)) and their exercise capacity according to the New York Heart Association classification (NYHA I-IV) and reassessed regularly after 3, 6 and 12 months. Thallium/Te MIBI scans at rest- and whenever possible at exercise as well as stress echocardiography are carried in the patients to assess symptomatic improvement, alterations in myocardial perfusion and functional efficacy by TMR. By intermediate analysis the 101 patients of our registry more than 60% of the patients had improved their angina class by at least one classe, some patients have improved perfusion as assessed by scintigraphy, which makes at present a trend but not yet a significant difference, whereas central hemodynamics and ejection fraction remained virtually unchanged in most patients reassessed after TMR. In our analysis mortality of the 101 TMR patients was assessed and plotted on Kaplan Meier survival curves. Mortality at 6 months was 11%. When compared to a historical group of patients with identical CCS and comparable NYHA classes, who were worked up in the manner of a case control study, the TMR mortality was marginally but not yet significantly lower than one would expect from these control patients with terminal CAD treated purely by medication: Their 6 months mortality was 14%. Remarkably but not unexpectedly patients with comparable CCS classes, who could still be treated by PTCA and/or CABG had a significantly lower 6 months mortality than TMR patients or patients on antianginal drugs only. The pathophysiological mechanisms for the symptomatic improvement by laser therapy are not yet fully understood. The 1 mm transmyocardial channels created by the CO2 laser have been postulated to permit perfusion from the ventricular cavity and to seek connection to capillaries and vessels present in the malperfused myocardium thus improving the perfusion by newly created connections and sinusoids from the ventricular cavity. Although there is clear evidence for the presence of open channels acutely and within a few days after TMR therapy little evidence in man is as yet available on the question whether the channels remain open in the long run and, if so, whether they can actually improve perfusion to a substantial degree...

Angioplasty, Balloon, Coronary↗
PubMed1996

[Transmyocardial laser revascularization--limits and possibilities].

Indications for interventional catheter techniques and bypass surgery have been extended to more complex lesions and also the number of reoperations after primary successful interventions has increased due to progression of the underlying disease. Finally a number of patients remains still symptomatic but, as a consequence of a very diffuse distribution of atherosclerotic lesions, is no longer accessible with conventional techniques of direct revascularization. This has drawn the attention again to indirect techniques of myocardial revascularization. Transmyocardial laserrevascularization offers a new option in reperfusing the ischemic myocardium via transmural channels from the ventricular cavity. As to the function of the channels, it is not quiet clear, wether they may connect to intramyocardial capillaries or may themselves induce a neoangiogenesis. However the clinical follow up in patients with intractable angina pectoris shows a significant improvement. At our hospital a number of 117 patients have been treated with this new method, 53 of them in conjunction with conventional bypass surgery. Clinical follow up after three and six months postoperatively showed a significant improvement concerning angina (CCS) and exercise tolerance (NYHA). This could also objectively be demonstrated by scintigraphy with an increased myocardial perfusion in 50% of the reinvestigated patients. Ischemic areas can still be seen, but occur at a significantly higher exercise level, demonstrating an improved but not normalized myocardial blood supply. The transmyocardial laserrevascularization is no alternative to well established procedures like PTCA or bypass surgery, but can be seen as a therapeutic option for those symptomatic patients recently being intractable. Further longterm studies and also experimental investigations have to evaluate the definitive role of this new treatment for endstage coronary heart disease.

Adult↗
PubMed1996

[Value of old and new electrocardiography criteria for differential diagnosis between ventricular tachycardia and supraventricular tachycardia with bundle branch block].

In 240 tachycardias with wide QRS-complex (> or = 120 ms), the value of the "old" ECG criteria published in 1978 by Wellens and coworkers was compared to the "new" ECG criteria published in 1991 by Brugada and coworkers for the differential diagnosis of tachycardias with wide QRS-complex. As main result of the study, it could be demonstrated that with the old as well as with the new ECG criteria a sensitivity of more than 90% for the correct diagnosis ventricular tachycardia can be reached. The specificity of the old and new ECG criteria for the diagnosis ventricular tachycardia is 70% and 72% for tachycardias with right bundle branch block configuration and 87% each for tachycardias with left bundle branch block configuration. The combined use of the old and the new ECG criteria in this study could not increase sensitivity and specificity for the diagnosis of ventricular tachycardia. Therefore, it does not appear to be important for the differential diagnosis of tachycardias with wide QRS-complex whether the old or the new step diagnostic criteria are being used, but that either the old or the new ECG criteria are being used correctly.

Adult↗
PubMed1995

Role of angiotensin II and prostaglandin E2 in regulating cardiac fibroblast collagen turnover.

In hypertensive heart disease, after myocardial infarction or in congestive heart failure, myocardial fibrosis presenting as a diffuse perivascular and interstitial accumulation of fibrillar collagens within the normal connective tissue structures of the myocardium is associated with an activated renin-angiotensin system (RAS). This reactive fibrosis occurs in the overloaded left ventricle and the nonoverloaded right ventricle irrespective of myocyte necrosis or the development of myocyte hypertrophy. Therefore, it appears that hemodynamic factors or the load of the ventricle are not primarily responsible for the adverse fibrous tissue response in the myocardium, and humoral factors may play a key role in regulating the myocardial collagen matrix. The neurohumoral response in hypertensive heart disease, after myocardial infarction with overall deterioration of left ventricular function or congestive heart failure leads to an activation of either the cardiac or the circulating RAS, which closely interacts with the bradykinin-prostaglandin system. To ascertain whether the RAS modulates collagen fibroblasts that express mRNAs for types I and III collagens (the major fibrillar collagens in the heart) and matrix metalloproteinase 1 (MMP1; the key enzyme for collagen degradation), collagen synthesis was measured by [3H]proline incorporation normalized to total protein synthesis and MMP1 activity was determined by degradation of [14C]collagen in cultured fibroblasts after 24-hour incubation with various concentrations of angiotensin II or PGE2 (10(-11)-10(-3) M) under serum-free conditions. In addition, effects of angiotensin II were evaluated in the presence or absence of either type 1 (ICI D8731) or type 2 (PD 123177) angiotensin II (AT1 or PGE2 (10(-11)-10(-3) M) under serum-free conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Whole mitochondrial genome amplification reveals basal level multiple deletions in mtDNA of patients with dilated cardiomyopathy.

Basal level multiple deletions in the heart mitochondrial (mt) DNA of patients with dilated cardiomyopathy were analyzed with the recently developed long PCR technique. The amplification of the whole mitochondrial genome and the length dependent preferential amplification ensure that all existing deletions are detected simultaneously. Primer shift long PCR proved the specificity of our method in the detection of deletions. We used primers that were 15644 bp and 13765 bp apart, which comprised almost the entire mitochondrial genome, detected a total of 14 kinds of deletions in 18 out of the 40 endomyocardial biopsy samples from patients with dilated cardiomyopathy. These deletions ranged in size from 3.3 kb to 12.6 kb. The proportion of the deleted to wild-type mtDNA was calculated to be less than 9% for any of these deletions. Aged patients had a comparatively higher proportion. Deletions were rarely found in mtDNA of leukocytes from the same group of patients and of 38 additional patients, as well as in myocardia of 25 normal controls (P < 0.01). No deletion was found in leukocytic mtDNA of the 21 control subjects. It is therefore concluded that cardiomyopathic heart has a high frequency of mtDNA deletions. With regard to the low quantity and the cumulative nature of these deletions by aging, they could have only little pathogenic effect on the development of dilated cardiomyopathy, but rather be a sign of increasing stress of the heart promoting the damage of mtDNA.

Base Sequence↗