Impact of the COVID-19 pandemic on cardiovascular mortality and catherization activity during the lockdown in central Germany: an observational study.

AIMS: During the COVID-19 pandemic, hospital admissions for cardiac care have declined. However, effects on mortality are unclear. Thus, we sought to evaluate the impact of the lockdown period in central Germany on overall and cardiovascular deaths. Simultaneously we looked at catheterization activities in the same region. METHODS AND RESULTS: Data from 22 of 24 public health-authorities in central Germany were aggregated during the pandemic related lockdown period and compared to the same time period in 2019. Information on the total number of deaths and causes of death, including cardiovascular mortality, were collected. Additionally, we compared rates of hospitalization (n = 5178) for chronic coronary syndrome (CCS), acute coronary syndrome (ACS), and out of hospital cardiac arrest (OHCA) in 26 hospitals in this area. Data on 5,984 deaths occurring between March 23, 2020 and April 26, 2020 were evaluated. In comparison to the reference non-pandemic period in 2019 (deaths: n = 5832), there was a non-significant increase in all-cause mortality of 2.6% [incidence rate ratio (IRR) 1.03, 95% confidence interval (CI) 0.99-1.06; p = 0.16]. Cardiovascular and cardiac mortality increased significantly by 7.6% (IRR 1.08, 95%-CI 1.01-1.14; p = 0.02) and by 11.8% (IRR 1.12, 95%-CI 1.05-1.19; p < 0.001), respectively. During the same period, our data revealed a drop in cardiac catherization procedures. CONCLUSION: During the COVID-19-related lockdown a significant increase in cardiovascular mortality was observed in central Germany, whereas catherization activities were reduced. The mechanisms underlying both of these observations should be investigated further in order to better understand the effects of a pandemic-related lockdown and social-distancing restrictions on cardiovascular care and mortality.

Swinging heart in acute pancreatitis.

Pleural effusions and ascites are not uncommon in acute pancreatitis; however, pericardial effusions complicated by cardiac tamponade are extremely rare and definite treatment has yet to be established. This case report illustrates the findings in a 57-year-old patient, who was diagnosed of an acute alcoholic pancreatitis. The clinical course was complicated by recurrent episodes of acute pancreatitis, and eventually, the patient developed acute circulatory failure that was caused by cardiac tamponade. The patient was successfully treated by an emergency pericardiocentesis; however, although the patient was treated with intrapericardial triamcinolone and octreotide, pericardial effusion reoccurred. Eventually, a pancreaticopericardial fistula was diagnosed by endoscopic retrograde cholangiopancreaticography, and after successful stent placement in a disrupted pancreatic duct, the clinical recovery was uneventful. To the best of the authors' knowledge, this is the first case of a successful endoscopic treatment of a pancreaticopericardial fistula complicated by cardiac tamponade in a patient with acute pancreatitis.

Enterococcus septicemia due to a pacemaker lead infection.

Pacemaker lead infections are rare but potentially life threatening. We report the case of an 80-year-old pacemaker-dependent female patient with complete heart block, who presented with subfebrile temperatures and chills due to a pacemaker lead infection by Enterococcus faecalis.

Clinical and immunologic characteristics in peripartum cardiomyopathy.

Peripartum cardiomyopathy (PPCM) is a rare disorder of dilated cardiomyopathy and left ventricular dysfunction occurring in the last month of pregnancy or within 5 months postpartum. Outcome of PPCM is highly variable, comprising clinical improvement and rapid deterioration unresponsive to medical treatment requiring heart transplantation or even death. In this study, we report the clinicopathologic findings of 10 patients with PPCM who were retrospectively identified in our cardiomyopathy registry. During a follow-up of 69+/-27 months, no patient died or required orthotopic heart transplantation. Left ventricular ejection fraction was 38+/-7% at the time of diagnosis and 53+/-7% during follow-up. While all patients had sinus rhythm at the time of diagnosis, three patients presented with left bundle branch block. We found no evidence of viral infection in endomyocardial biopsy samples of seven patients by PCR. Histopathologic findings revealed the presence borderline myocarditis in two of seven patients (29%). Circulating autoantibodies to cardiac tissue of any kind were observed in all patients. In conclusion, in our retrospective observational study, no patient diagnosed with PPCM died or received orthotopic heart transplantation. Improvement of left ventricular ejection fraction was present in eight patients (80%), while LV dysfunction persisted in four patients. Our findings support the hypothesis of an underlying autoimmune pathomechanism in this rare disease.

Matrix metalloproteinases and their inhibitors in malignant and autoreactive pericardial effusion.

Matrix metalloproteinases (MMPs) are proteolytic enzymes essentially involved in tissue remodeling and tumor invasion, and their activity is counterbalanced by endogenous antagonists, the tissue inhibitors of matrix proteinases (TIMPs). Recent reports have suggested a potential role of MMPs in the evolution of pericardial effusion (PE). In this study, we determined the levels of MMP-2 and MMP-9 and their inhibitors TIMP-1 and TIMP-2 in 19 patients who had malignant PE that was confirmed by histology or cytology and 30 patients who had nonmalignant, autoreactive PE compared with pericardial fluid of 19 patients who had preserved left ventricular function and who underwent aortocoronary bypass surgery for control. Samples were assayed by zymography, immunoblotting, and quantitative enzyme-linked immunosorbent assay. We found significantly higher MMP-2 levels in malignant PE than in pericardial fluid (2,906 +/- 348 vs 1,493 +/- 114 ng/ml, p = 0.0005) or autoreactive PE (2,079 +/- 269 ng/ml, p = 0.01). No significant differences in MMP-9 levels were found between malignant PE and autoreactive PE (83 +/- 28.6 vs 106 +/- 30.4 ng/ml, p = 0.22), whereas MMP-9 was below the detection limit in pericardial fluid. No differences in TIMP-1 levels were found across the different study groups, whereas compared with pericardial fluid, TIMP-2 levels were significantly lower in autoreactive PE (113 +/- 18.9 vs 187 +/- 12.2 ng/ml, p = 0.002). In addition, there was a trend to lower TIMP-2 levels in malignant PE (137 +/- 27.1 ng/ml, p = 0.07). The present findings indicate that proteolytic enzymes and their inhibitors are involved in the pathogenesis of PE, with an expression pattern that depends on etiology. The involvement of MMP-2 in the pathogenesis of malignant PE may indicate a potential role of MMP inhibitors in the control of malignant PE.

Predictive value of high-sensitivity C-reactive protein in patients with idiopathic dilated cardiomyopathy.

We analyzed the serum concentrations of high-sensitivity C-reactive protein (hsCRP) at the time of diagnostic cardiac catheterization in 198 patients with idiopathic dilated cardiomyopathy (IDC) to evaluate its prognostic value. Patients were dichotomized according to a median value of hsCRP of 2 mg/dL. Predefined study endpoints over 69 +/- 33 months of follow-up included major arrhythmic events and transplant-free survival. Major arrhythmic events during follow-up occurred in 20 of 98 patients (20%) with low, compared to 22 of 100 patients (22%) with high hsCRP (ns). By multivariate analysis, a depressed left ventricular ejection fraction (LVEF) was the only significant predictor of arrhythmic risk. Death or cardiac transplantation was observed in 36% of patients with high, versus 22% of patients with low hsCRP (P < 0.05). By multivariate analysis, hsCRP and LVEF were independent predictors of transplant-free survival. Thus, in this patient population with IDC, hsCRP had independent prognostic value with regard to transplant-free survival, but did not contribute in the stratification with regard to arrhythmic risk.

Acute parvovirus B19 infection associated with myocarditis in an immunocompetent adult.

Inflammatory heart disease is causally linked with progressive left ventricular dysfunction and congestive heart failure. In childhood, infection with parvovirus B19 (PVB19) is usually benign, causing erythema infectiosum. However, severe fetal PVB19 infection may be associated with hydrops fetalis and fetal death caused by myocarditis. Here we report a PVB19-induced myocarditis in a previously healthy 37-year-old patient admitted to the hospital because of chest pain and dyspnea due to left ventricular dysfunction. Four weeks after the onset of symptoms, we found lymphocytic infiltrates and PVB19 genome in left ventricular endomyocardial biopsy specimens. Consistently, acute PVB19 infection was indicated serologically by elevated IgM titers and the presence of PVB19 genome in peripheral blood lymphocytes. In conclusion, PVB19 infection may be complicated by acute myocarditis in immunocompetent adults. Because PVB19 myocarditis may progress to chronic dilated cardiomyopathy, early diagnosis by endomyocardial biopsy is important to initiate anti-inflammatory treatment.

[Pregnancy and cardiomyopathies]. / Schwangerschaft und Kardiomyopathie.

This overview on the topic of cardiomyopathy and gestation comprises the diagnostic and therapeutic options of patients with preexistent cardiomyopathies (dilated, hypertrophic, inflammatory, and others) and with cardiomyopathies which have been discovered during or in the 6 months following delivery. CARDIOMYOPATHIES PREEXISTENT BEFORE GESTATION: If cardiomyopathy is present before an intended gestation, the couple should be advised against pregnancy because of the high risk of deterioration both during gestation and peripartum. If pregnancy occurs, according to ESC (European Society of Cardiology) recommendations termination should be advised if the ejection fraction is < 50% and/or the LV dimensions are definitely above normal. If termination is refused, the patient must be checked regularly by both gynecologist and cardiologist, by the latter to perform regular echocardiograms. Termination is not recommended for the hypertrophic (nonobstructive) cardiomyopathies. If atrial fibrillation occurs, anticoagulation with low molecular weight heparin and digoxin and/or Betablockers are recommended for rhythm and rate control. PERIPARTUM CARDIOMYOPATHIES: In peripartum cardiomyopathies, which are discovered clinically postpartum, inflammation of the myocardium sometimes associated with pericarditis is frequently found. For those patients, we recommend heart catheterization with endomyocardial biopsy to allow for the exact diagnosis of the underlying cardiac process (inflammatory and/or viral vs autoreactive myocarditis or noninflammatory or nonviral [= idiopathic] forms). This diagnostic algorithm, which we recommend for any form of dilated cardiomyopathy, bears impact on treatment options beyond the mere heart failure therapy that should be instigated anyhow.

Doxycycline and tissue repair in rats.

Iterations in collagen turnover are integral to tissue repair. Repair gone awry, as a result of excess collagen accumulation or degradation, can contribute to pathologic ventricular remodeling. Pharmacologic interventions that would attenuate either aspect of faulty repair have therefore attracted interest. Tetracyclines, which inhibit both collagen synthesis and degradation, as well as angiogenesis, may hold promise, unrelated to their antimicrobial properties, in this regard. Assessment of their potential in rodent hearts with experimental injury can be problematic, given the often microscopic nature of tissue repair and brief involvement of matrix metalloproteinases (MMPs). We therefore selected a subcutaneous model in which granulation and fibrous tissues form over several weeks in response to croton oil and where fibrous tissue is subsequently resorbed because of high levels of collagenolytic activity. Untreated rats were compared with those given daily oral doxycycline (40 mg/kg). We harvested pouch tissue and exudate weekly for 5 weeks to assess hydroxyproline concentration and MMP activity (gelatin substrate zymography) of pouch wall and mononuclear cell count of pouch exudate. At week 2, neovascularization in pouch wall was measured by means of intravenous infusion of carmine-red dye in gelatin. The resultant "vascular cast" was solubilized and dye content quantitated with the use of spectrophotometry. Serum was assayed weekly for type I collagen carboxyterminal telopeptide (ICTP), a marker of collagen degradation. During weeks 1 and 2 and compared with untreated controls, doxycycline-treated rats had attenuated pouch tissue weight, collagen concentration, MMP2 lytic activity and vascularity, and reduced exudate volume and mononuclear cells. In vitro, doxycycline inhibited tissue gelatinolytic activity in a dose-dependent manner. At weeks 4 and 5, pouches were larger and collagen concentration was higher in doxycycline-treated rats, and serum ICTP levels were reduced at weeks 3 and 4. During the initial phase of pouch development, doxycycline exerts an inhibitory effect on tissue formation, likely mediated through its attenuation of angiogenesis and modulations of collagen turnover. As repair proceeds in subsequent weeks, doxycycline retards collagen degradation and pouch resorption by inhibiting MMPs. Doxycycline offers a multifaceted pharmacologic profile with which to modify various aspects of tissue repair in the rat.