scholarly journals Myocarditis and Subclinical-Like Infection Associated With SARS-CoV-2 in Two Cats Living in the Same Household in France: A Case Report With Literature Review

2021 ◽  
Vol 8 ◽  
Author(s):  
Valérie Chetboul ◽  
Pierre Foulex ◽  
Kahina Kartout ◽  
Anne Marie Klein ◽  
Corinne Sailleau ◽  
...  

This report provides the first clinical, radiographic, echocardiographic, and biological description of SARS-CoV-2-associated myocarditis with a 6-month follow-up in a 5-year-old obese male domestic shorthair cat (Cat-1) presented for refractory congestive heart failure, with high cardiac troponin-I level (5.24 ng/ml), and a large lingual ulcer. The animal was SARS-CoV-2 positive on serology. The other cat living in the same household (Cat-2) never showed any clinical sign but was also confirmed SARS-CoV-2 positive on serology. Both cats were SARS-CoV-2 PCR negative. Cat-1 had closer contact than Cat-2 with their owner, who had been in close contact with a coworker tested PCR positive for COVID-19 (Alpha (B.1.1.7) variant) 4 weeks before Cat-1's first episode of congestive heart failure. A focused point-of-care echocardiography at presentation revealed for Cat-1 numerous B-lines, pleural effusion, severe left atrial dilation and dysfunction, and hypertrophic cardiomyopathy phenotype associated with focal pulmonary consolidations. Both myocarditis and pneumonia were suspected, leading to the prescription of cardiac medications and antibiotics. One month later, Cat-1 recovered, with normalization of left atrial size and function, and radiographic and echocardiography disappearance of heart failure signs and pulmonary lesions. An extensive literature review of SARS-CoV-2-related cardiac injury in pets in comparison with human pathology is discussed.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Rashad J Belin ◽  
Steve Mottl ◽  
Jacob Goldstein ◽  
Abigail Angulo ◽  
Ashima Salwan ◽  
...  

Background: The sympathetic nervous system (SNS) is thought to play an important role in promoting atrial fibrillation (AF) initiation and maintenance, especially in the setting of congestive heart failure (CHF). However, it is unclear as to which components of the SNS are altered in atria isolated from failing hearts. These studies are essential, as they will delineate potential molecular targets that may be probed for therapeutic intervention in order to reduce AF pathogenesis. Methods : CHF was induced by ventricular tachypacing (240 beats/minute) for 4 weeks in hound dogs. A total of 4 CHF and 5 control dogs were used. Immunoblot analysis was performed on left atrial appendage (LAA) homogenates to examine the protein expression of Gsα, Gi2α, and the catalytic subunit of protein kinase A (PKA). Catalytic activities of PKA and protein phosphatase type 2a (PP2a) were determined using non-radioactive enzyme activity assay systems. Cyclic AMP (cAMP) accumulation was assessed by an enzyme linked immunoabsorbant assay and phosphorylation of cardiac troponin I (cTnI) was determined using a phosphospecific antibody against cTnI. Results: Gsαconcentrations were increased approximately 4-fold in failing left atrial preparations relative to control. In contrast, expression of Gi2αwas modestly increased ~1-fold in failing LAA relative to non-failing atrial muscles. PKA activity was significantly increased in failing LAA preparations compared to control (124.7 vs. 42.1 pmole phosphate/minute, P <0.05); while, PP2a activity was substantially decreased in failing LAA (4.60 vs. 7.06 pmole phosphate/μg protein/minute, P <0.05). cAMP concentrations were increased and expression of the catalytic subunit of PKA was upregulated (~1.5-fold increase) in failing LAA. Lastly, phosphorylation of cardiac troponin I (cTnI) was enhanced in failing LAA preparations. Conclusions: Our data are the first to characterize sympathetic remodeling in left atrial muscles isolated from an experimental model of CHF. Additionally, our results support the hypothesis that augmented sympathetic signaling and activation may contribute to the AF substrate in a canine model of CHF characterized by increased AF susceptibility.


2020 ◽  
Author(s):  
Tarun Dalia ◽  
Shubham Lahan ◽  
Sagar Ranka ◽  
Prakash Acharya ◽  
Archana Gautam ◽  
...  

Background: Coronavirus disease 2019 (COVID-19) has been reported to cause worse outcomes in patients with underlying cardiovascular disease, especially in patients with acute cardiac injury, which is determined by elevated levels of high-sensitivity troponin. There is a paucity of data on the impact of congestive heart failure (CHF) on outcomes in COVID-19 patients. Methods: We conducted a literature search of PubMed/Medline, EMBASE, and Google Scholar databases from 11/1/2019 till 06/07/2020, and identified all relevant studies reporting cardiovascular comorbidities, cardiac biomarkers, disease severity, and survival. Pooled data from the selected studies were used for metanalysis to identify the impact of risk factors and cardiac biomarker elevation on disease severity and/or mortality. Results: We collected pooled data on 5,967 COVID-19 patients from 20 individual studies. We found that both non-survivors and those with severe disease had an increased risk of acute cardiac injury and cardiac arrhythmias, our pooled relative risk (RR) was - 8.52 (95% CI 3.63-19.98) (p<0.001); and 3.61 (95% CI 2.03-6.43) (p=0.001), respectively. Mean difference in the levels of Troponin-I, CK-MB, and NT-proBNP was higher in deceased and severely infected patients. The RR of in-hospital mortality was 2.35 (95% CI 1.18-4.70) (p=0.022) and 1.52 (95% CI 1.12-2.05) (p=0.008) among patients who had pre-existing CHF and hypertension, respectively. Conclusion: Cardiac involvement in COVID-19 infection appears to significantly adversely impact patient prognosis and survival. Pre-existence of CHF and high cardiac biomarkers like NT-pro BNP and CK-MB levels in COVID-19 patients correlates with worse outcomes. Keywords: Acute cardiac injury; cardiac arrhythmia; mortality risk; cardiac biomarkers, COVID-19.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sandeep Singh ◽  
Akhil Jain ◽  
Priyanka Chaudhari ◽  
Faizan Ahmad Malik ◽  
Virmitra Desai ◽  
...  

Introduction: COVID-19 has been linked to cardiac damage and life-threatening pericardial complication on which data are trivial which incited us to perform this review of published case reports. Methods: PubMed/Medline, Web of Science and SCOPUS were searched until June 2020 for case reports on COVID-19-associated pericarditis, cardiac tamponade or pericardial effusion. Results: We identified 8 articles reporting 11 COVID-19 positive cases [mean age: 51.4±14.3 (34-78 yrs) 5 male/6 female)] with pericardial complications. All (100%) cases were COVID-19 positive at the presentation with ~80% having dyspnea, chest pain and cough. Time interval from first symptom to pericardial effusion was 7±8 (1-26) days. Five patients reported heart failure with reduced EF on echocardiography with mean LVEF 36.25%±8.54%. All patients showed nearly normal Troponin-I without angiographically significant stenosis except one. Out of 8 cases on echocardiography 4 cases reported with diffuse hypokinesia, 2 reported inferior and inferolateral walls hypokinesia and 2 reported signs of pericardial tamponade. Out of 11 patients, cardiovascular risk factors in the form of diabetes or hypertension or obesity were present in 5 patients. Cardiovascular comorbidities such as heart failure with low ejection fraction, non-ischemic cardiomyopathy and prior myocarditis were present in 3 patients. ST-segment elevation in 3, sinus tachycardia in 2, T wave inversion in 1 case were noted. Four patients developed cardiac tamponade, 1 developed takotsubo syndrome and 3 patients died. Conclusions: COVID-19 patients had signs of a high burden of cardiac injury. Pericardial complications (pericardial effusion and cardiac tamponade) remain infrequent complications which may require prompt care to avoid mortality.


1979 ◽  
Vol 236 (4) ◽  
pp. H554-H560 ◽  
Author(s):  
I. H. Zucker ◽  
L. Share ◽  
J. P. Gilmore

The renal response to left atrial balloon inflation in normal dogs was compared with that in dogs with chronic congestive heart failure (CHF). CHF was induced by the production of an aortocaval fistula below the level of the renal arteries. CHF dogs showed elevated left ventricular end-diastolic pressure, enlarged hearts, a depression of myocardial contractility, pulmonary edema, ascites, and peripheral edema. They also showed significant decreases in urine flow, creatinine clearance, para-aminohippurate clearance, sodium and potassium excretion, fractional sodium excretion, osmolar clearance, arterial blood pressure, and heart rate. Balloon distension of the left atrium evoked a significant increase in urine flow and free-water clearance in the normal group. The reflex nature of this response was indicated by its blockade after bilateral cervical vagotomy. In contrast, the CHF group did not exhibit significant changes in urine flow or free-water clearance during balloon inflation. Plasma antidiuretic hormone (ADH) was significantly elevated in the CHF group; however, balloon distension reduced plasma ADH in both groups of dogs. Plasma renin activity was significantly elevated in the CHF dogs and was not changed by balloon distension in either group of dogs. It is concluded that animals with high-output CHF do not exhibit the atrial-diuretic reflex in spite of their ability to reduce ADH levels by atrial distension.


2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Manuel Rodríguez Martínez ◽  
Eladio Ruiz González ◽  
Anna Parra-Llorca ◽  
Máximo Vento Torres ◽  
Marta Aguar Carrascosa

Neonatal acute myocardial infarction is an uncommon entity. We describe the case of a 4-day-old term baby who presented with respiratory distress and distal acrocyanosis. The chest radiograph demonstrated cardiomegaly without pleural effusion, and examination revealed hepatomegaly. An electrocardiogram revealed QS pattern in leads I, aVL, and V6, suggestive of ischemia. Cardiac enzymes were elevated, and echocardiogram revealed moderate left ventricular dysfunction with a thrombus at the level of the left atrial appendage. The patient required hemodynamic stabilization, vasodilatation to avoid congestive heart failure, and anticoagulation with heparin and aspirin. In the context of this unusual diagnosis, we reviewed our experience over the last 17 years as well as the existing literature on neonatal myocardial infarction.


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