Clinical significance of intrinsic sympathomimetic activity of the beta blocker carteolol. II: Comparative studies of carteolol and pindolol in patients with bradycardia

Completing previous studies in patients with sinus bradycardia (Med. Klin. 82 [1987], 647-650) we compared metoprolol with carteolol and pindolol, pindolol with carteolol, no treatment with carteolol (in two groups) in five series of the paired comparisons of Holter-ECG each. With change from metoprolol to carteolol or pindolol (dose ratio 10:1) lowest heart rate on Holter-ECG increased by 28 or 29% without change of exercise heart rate. Direct comparison of pindolol and carteolol revealed a very similar heart rate profile, indicating equipotent beta blockade and ISA. In patients with previous beta blocker induced bradycardia, carteolol did not change a normal resting heart rate off treatment. However, in patients with spontaneous sinus bradycardia carteolol increased lowest heart rate (+14%, due to overriding ISA) and lowered exercise heart rate (-15%, due to overriding beta blockade). A beta blocker induced sinus bradycardia consistently improved with change of treatment to carteolol and pindolol. With caution carteolol and pindolol may also be used despite spontaneous sinus bradycardia.     

Arrhythmogenic right ventricular cardiomyopathy: a cause of sudden death in young people

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an increasingly recognized cause of ventricular tachycardia and sudden cardiac death in young people, notably young athletes. The best treatment is not clear, although options include antiarrhythmic drugs, radiofrequency ablation, and implantable defibrillators.     

Predictive role of C-reactive protein in sudden death: a meta-analysis of prospective studies

ObjectiveC-reactive protein (CRP) is a powerful predictor of and risk factor for cardiovascular disease. However, the relationship between CRP and sudden death (SD) is controversial. Therefore, we performed a meta-analysis to evaluate the association between CRP and SD.MethodsWe conducted a comprehensive search of the databases of PubMed, Web of Science, Embase, Cochrane Library, Wanfang, CNKI, China Biology Medicine disc, and Weipu. Two researchers independently screened the literature, extracted data, and evaluated the data quality. The overall effect size was meta-analyzed using Stata software version 12.0 (StataCorp, College Station, TX, USA).ResultsTwelve prospective studies involving 36,646 patients were included in the present meta-analysis. The data revealed that patients with higher CRP concentrations had a greater risk of SD (hazard ratio, 1.19; 95% confidence interval, 1.09–1.29). When the hazard ratio of SD was calculated by multivariate analysis of nine studies, CRP was confirmed to be an independent predictive factor for SD (hazard ratio, 1.05; 95% confidence interval, 1.03–1.07).ConclusionsThis meta-analysis confirmed that CRP is an independent predictor of SD. These results support the recommendation of recording the CRP concentration for risk assessment of SD in clinical practice.     

Tigecycline exhibits inhibitory activity against Clostridium difficile in the colon of mice and does not promote growth or toxin production

Tigecycline is a broad-spectrum glycylcycline antibiotic with potent in vitro activity against Clostridium difficile. We used a mouse model to test the hypothesis that tigecycline has a low propensity to promote colonization and toxin production by C. difficile due to inhibitory activity in the colon. Mice (5 to 8 per group) received subcutaneous injections of tigecycline (low and high doses) alone or in combination with clindamycin for 6 days. Growth of and toxin production by 3 strains of C. difficile (tigecycline MICs ≤ 0.012 μg/ml) were measured in cecal contents collected 6 h or 3 days after the final antibiotic dose. Antibiotic concentrations were measured using a bioassay, and concentrations of total anaerobes and Bacteroides spp. were measured. The effects of tigecycline on rendering mice susceptible to colonization with and reducing the burden of C. difficile were also examined. In comparison to saline controls, clindamycin promoted the growth of C. difficile (P < 0.001) in cecal contents, whereas tigecycline did not. Tigecycline did not suppress total anaerobes or Bacteroides spp. in comparison to saline controls. Concurrent administration of tigecycline prevented clindamycin-induced promotion of C. difficile in cecal contents collected 6 h or 3 days (high dose only) after the final antibiotic dose. Tigecycline did not promote the establishment of colonization in mice, yet it did not reduce concentrations of C. difficile in animals with established colonization. In summary, tigecycline did not promote the growth of or toxin production by C. difficile, probably due to inhibitory activity against C. difficile and relative sparing of indigenous anaerobic microflora.     

Nonsustained, asymptomatic ventricular tachycardia in patients with coronary artery disease: prognosis and incidence of sudden death of patients who are noninducible by electrophysiological testing

The objective of this study was to determine the long-term prognosis and the sudden death risk for patients with coronary artery disease and spontaneous nonsustained ventricular tachycardia who are not inducible by electrophysiological testing. Patients with coronary artery disease (CAD) who have spontaneous or inducible sustained ventricular tachycardia (VT) by electrophysiological testing are at increased risk of dying suddenly, and noninducibility is often considered as a favorable prognostic factor in their risk assessment. We studied 120 consecutive patients with CAD and nonsustained VT during Holter monitoring and followed the patients who were noninducible (n = 93) for 3.5 +/- 1.6 years. None of these patients received antiarrhythmic therapy except beta-blockade. Overall mortality and the sudden death risk was assessed by the Kaplan-Meier estimation. Predictors for overall mortality and sudden death were determined by multivariate analysis. During follow-up, 23 of the 93 patients died, including 13 suddenly. Overall mortality was 9% after 1 year, 16% after 2 years, and 21% after 3 years, respectively. The incidence of sudden death was 1% after 1 year, 8% after 2 years, and 13% after 3 years, respectively. Patients with a LVEF < or = 0.35 had an increased overall mortality risk with 15% after 1 year, 29% after 2 years, and 34% after 3 years (P = 0.012) and a risk of dying suddenly of 4% after 1 year, 12% after 2 years, and 18% after 3 years (P = NS), respectively. LVEF was the only independent predictor for overall mortality. In conclusion, patients with coronary artery disease and nonsustained ventricular tachycardia who are not inducible by electrophysiological testing have a moderate long-term overall mortality risk. The risk of dying suddenly in this patient group is small but not negligible, especially in patients with impaired LVEF.     

An autopsy case of COVID‐19 with a sudden death: Clinico‐pathological comparison

Autopsy was performed on a COVID‐19 patient, who suddenly died despite the extensive anti‐viral and anti‐inflammatory therapies. Although moderate subpleural fibrosis was seen, pathology of DAD, a well‐known cause for pulmonary failure, was minimum. Instead, severe hemorrhage was observed. Therapeutic effects were indicated; however, why severe hemorrhage occurred was unclear.     

Aborted sudden death in a patient with a structurally normal heart: the Brugada syndrome

We report a 37-year-old man with documented aborted sudden death. After resuscitation, the patient showed no structural heart disease but the ECG showed a right bundle-branch block with a descending ST segment elevation in leads V(1) and V(2). After transient normalization of the ECG, the administration of ajmaline led to spontaneous development of the distinct descending ST segment elevation in the right precordial leads and therefore to the diagnosis of Brugada syndrome. The incidence of sudden cardiac death among these patients is high. The only treatment is an implantable cardioverter-defibrillator (ICD). The Brugada syndrome should therefore be borne in mind in the differential diagnosis of sudden death.     

When the safe place does not protect: reports of victimisation and adverse experiences in psychiatric institutions

Psychiatric patients report higher levels of victimisation and are at risk for further victimisation in different contexts, such as psychiatric institutions. Studies in this field tend to focus on hospital staff as victims, experiencing classic forms of victimisation (e.g. physical assault, threats, verbal abuse), through qualitative studies. This is a quantitative retrospective study that aims to know the occurrence of psychiatric victimisation and other adverse experiences in Portuguese psychiatric patients. Ninety‐five psychiatric patients, between 20 and 79 years old (M – 45.18, SD – 13.06), with a history of psychiatric hospitalisation answered the Experiences in Psychiatric Institution Inventory. Participants were recruited in four psychiatric hospitals. Inpatients were approached during their hospitalisation; outpatients were approached in scheduled appointment days. Only 23 (24.2%) participants reported no victimisation. Total Experiences of Self varied from 0 to 7 (M – 1.75, SD – 1.72), Total Witnessed Experiences varied from 0 to 7 (M – 1.17, SD – 1.64), and Total Global Experiences varied from 0 to 14 (M – 2.92, SD – 3.01). These results show that victimisation and adverse experiences in psychiatric contexts are frequent and go beyond classic forms of victimisation. A deeper knowledge of these experiences and their impact in the mental health of psychiatric patients may promote quality of care provided and lead to more effective treatments, thus reducing the number and length of hospitalisations, and the financial burden for public health services.     

Addition of a defibrillation electrode in the low right atrium to a right ventricular lead does not reduce ventricular defibrillation thresholds

Transvenous unipolar active can defibrillation systems have proven to be effective in treating ventricular tachyarrhythmias. However, a further reduction of ventricular defibrillation thresholds (V-DFT) would increase the longevity, reduce the size of pulse generators, and help to avoid additional leads in patients with inacceptable high V-DFTs. In a finite difference computer model, the extension of the right ventricular (RV) defibrillation coil into the low right atrium led to a 40% reduction of unipolar V-DFT. To evaluate this finding, we conducted a prospective, randomized study in 11 patients receiving an ICD. Extension of the RV electrode was simulated by adding a second coil placed in the low right atrium with the same polarity. Using a binary search protocol, V-DFT was determined with and without the additional electrode in each patient. Total shock impedance was significantly lower in the two coil (low RA) configuration, compared to the single coil (RV) configuration. Corresponding values were 49.9 +/- 6.7 Ohm and 61.1 +/- 9.3 Ohm, respectively (P < 0.01, paired t-test). However, there was no reduction, but even a nonsignificant increase in V-DFTs. Mean V-DFT in the RV configuration was 12.0 +/- 5.6 J and 16.3 +/- 7.8 J in the low RA configuration (P = 0.09, paired t-test). Despite a reduction in total impedance, the addition of a defibrillation coil in the low right atrium does not reduce ventricular defibrillation thresholds.     

Ranolozine-induced suppression of ventricular tachycardia in a patient with nonischemic cardiomyopathy: a case report

Ranolazine is an antianginal agent, which inhibits the abnormal inward Na⁺ current and by this inhibition decreases diastolic cardiomyocyte calcium levels and improves electrical stability. Ranolazine has also been shown to be a potent inhibitor of after depolarizations and triggered activity. In this case report, we describe the dramatic antiarrhythmic effects of ranolazine in a patient with nonischemic cardiomyopathy who had malignant ventricular tachycardia. Further research on the antiarrhythmic properties of ranolazine appears warranted.     

In-vitro activity of coumermycin against methicillin-resistant staphylococci: a comparison with six other agents

The in-vitro activity of coumermycin was compared with that of vancomycin, rifampicin, fusidic acid, trimethoprim-sulphamethoxazole, norfloxacin and cefamandole against seven isolates of methicillin-resistant Staphylococcus aureus and 97 isolates of methicillin-resistant coagulase negative staphylococci. Apart from one strain of methicillin-resistant S. aureus all isolates were inhibited by less than or equal to 0.06 mg/l of coumermycin. Cefamandole was more active against strains of S. epidermidis than against other coagulase negative staphylococci.     

Moxifloxacin: a comparison with other antimicrobial agents of in-vitro activity against Streptococcus pneumoniae

Two hundred representative isolates, including 26 strains of Streptococcus pneumoniae with intermediate resistance to penicillin, were selected from a collection obtained from blood cultures of patients with bacteraemic pneumococcal pneumonia. The MICs of moxifloxacin (BAY 12-8039), grepafloxacin, sparfloxacin, levofloxacin, ofloxacin, ciprofloxacin, erythromycin, tetracycline and penicillin G were determined by a standard agar dilution technique. Moxifloxacin had the highest in-vitro activity against S. pneumoniae (MIC90 = 0.25 mg/L; MIC range 0.06-0.25 mg/L). The MIC90 values were one dilution lower than those obtained with sparfloxacin and grepafloxacin, three dilutions lower than those obtained with levofloxacin, and four dilutions lower than those of ofloxacin and ciprofloxacin.