Cardiac biomarkers and mortality in COVID-19 infection: A review.

Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), creatine kinase-myocardial band (CK-MB) and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. The purpose of this review is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes.

Endothelial dysfunction in COVID-19 patients assessed with Endo-PAT2000.

It has been widely reported that the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) attaches human cells by using the Angiotensin Converting Enzyme 2 (ACE2) receptor, but vascular impairment described during coronavirus disease 2019 (COVID-19) infection is primarily due to the direct involvement of the endothelial cells by the virus or secondarily to the inflammatory host response is currently unknown. We therefore aimed to demonstrate in vivo the presence of endothelial dysfunction in six COVID-19 patients without cardiovascular risk factors or pre-existing cardiac condition, using the Endo-PAT 2000, a device able to measure endothelial vasodilation function in a rapid and non-invasive way. Four patients were positive for endothelial dysfunction, with RHI values between 1.13-1.56 (average value 1.32, normal values >1.67); in one of the two negative patients the reported RHI value was slightly above the cutoff (1.72). Our findings confirm that COVID-19 patients are at higher risk of developing endothelial dysfunction. In addition, our results demonstrate that endothelial impairment may occur even in the absence of cardiovascular risk factors.

Impact of RAAS Inhibitors on Clinical Outcome and Mortality in Patients With STEMI During the COVID-19 Era: A Multicenter Observational Study

Conflicting results are available regarding the influence of ACEi/ARBs on the risk of COVID-19 infection, while less is known about their impact on the clinical outcome of patients with STEMI diagnosed with COVID-19. Our aim was to evaluate the impact of ACEi/ARBs therapy on in-hospital mortality and clinical outcomes of patients with STEMI during the COVID-19 pandemic. We retrospectively analyzed consecutive patients with STEMI hospitalized from February 20 to May 10, 2020 in four Hospitals in Lombardy. SARS-COV-2 diagnosis was performed by nasopharyngeal swab test. Procedural outcome, respiratory complications, and in-hospital mortality were reported. Univariate and multivariate analyses were performed by logistic regressions. Our population was represented by 182 patients with STEMI, 76.9% of which were males, and mean age was 67 ± 12.5. Hypertension was reported in 53.3%, and 29.1% was treated with ACEi/ARBs. COVID-19 diagnosis was confirmed in 17.1% of the patients. In-hospital mortality (13.2%) was significantly higher in patients with COVID-19 (31 vs. 10%, p = 0.003), even if ejection fraction [OR 0.93 (95% CI) 0.87–0.99;p = 0.03] and respiratory complications [OR 9.39 (95% CI) 1.91–45.9;p = 0.006] were the only two independent predictors. The incidence of COVID-19 infection was not influenced by ACEi/ARBs (16.5 in naïve vs. 18.8%) whose presence on admission did not correlate with respiratory complications or mortality both in the case of discontinuation and maintenance. In conclusion, in a high-risk population, such as that of patients with STEMI, the potential benefit of ACEi/ARB discontinuation in patients with COVID-19 is overcome by its detrimental effect. Intensive care, additional preventive respiratory investigations, regardless of swab test result, should be suggested for all patients admitted for STEMI during the pandemic.

Cardiac involvement in a 23 years old patient with granulomatosis with polyangiitis (GPA)

Aims Granulomatosis with polyangiitis (GPA) is a systemic necrotizing vasculitis, which could potentially affect any organ system. However, there have only been a few reports on cardiac involvement. In fact, it most commonly involves the sinuses, lungs, and kidneys with necrotizing granulomatous vasculitis. In 12% of a large series of patients with GPA there was cardiac involvement, largely manifested by pericarditis and coronary arteritis. Methods and results We describe a rare case of a 23-year-old girl, with no pathological history, at exception of a recent flu-like syndrome for which she carried out the search for SARS-CoV-2 RNA through nasopharyngeal swab, results negative. After a month, she went to the emergency department for a syncopal episode and subsequent head trauma. On this occasion, echocardiogram performed showed the presence of left ventricular systolic dysfunction due to hypokinesia of the middle distal segments;CT angiography of the chest revealed the presence of pulmonary embolism. For this reason, the patient was admitted to the cardiac intensive care unit, where EKG shown anterolateral myocardial infarction with ST elevation and immediately was performed coronary angiography, that evidenced two-vessel disease, with subsequent ineffective attempt to angioplasty. Due to the intercurrent appearance of hyposthenia and paraesthesia in the left upper limb, CT angiography of the brain was performed with detection of lower right pre central frontal hypodensity, suspected for recent ischaemic lesion and hypodensity of the right carotid artery as recent thrombosis. In light of the multi-organ involvement of ischaemic nature and the young age of the patient, rheumatological evaluation was carried out, with execution of a laboratory tests that showed the presence of positivity for ANCA anti-PR3 antibodies, on the basis of which was diagnosed GPA, and rituximab therapy was immediately initiated, with clinical benefit. Conclusions Cardiac involvement of GPA was first reported by Wegener in 1936. Classical or generalized GPA is characterized by necrotizing granulomatous vasculitis of the upper and lower respiratory tract together with glomerulonephritis. Widespread disseminated vasculitis involving both small arteries and veins occurs to a greater or lesser degree as the disease progresses. A localized form of GPA limited primarily to the upper and lower respiratory tracts has been described. Despite histopathological diagnosis of GPA, with autoantibodies against to circulatory neutrophilic cytoplasmic antigens, we can diagnose GPA easily and early. GPA must be kept in mind as the differential diagnosis of new onset cardiomyopathy, especially in the existence of pulmonary and renal pathologies. The clinical presentation of GPA can be so diverse that the list of differential diagnoses is vast, ranging from infections (fungal, bacterial, and mycobacterial) to other vasculitides, including Henoch–Schönlein purpura, sarcoidosis, Behcet syndrome, and malignancies. Despite that involving the heart is well described, significant cardiac complications occurring during the course of the disease are rare.

SARS-CoV-2 associated myopericarditis in a patient with previous myocarditis

Aims Severe acute respiratory syndrome coronavirus (SARS-CoV-2) is well described as being responsible for multi-organ involvement and SARS-CoV-2 cardiac involvement was observed since the beginning of the spread of the infection. However, there are no descriptions of acute myopericarditis in patient with previous myocarditis. Methods and results Cardiac involvement was assessed with electrocardiographic and echocardiographic changes and with increased levels of cardiac high-sensitivity troponin T (hs-cTnT). Diagnosis was confirmed with cardiac magnetic resonance imaging (CMR) and coronary artery disease (CAD) was excluded with coronary angiography. A 53-years-old woman with hypokinetic cardiomyopathy due to a previous myocarditis and recent COVID-19 pneumonia reached the Emergency Department with chest pain and tachycardia in December 2020. Twelve-lead ECG was not conclusive and after detection of significative increase of hs-cTnT she was admitted to the Cardiology Department. Transthoracic echocardiography showed reduction of left ventricle ejection fraction, subendocardial bright appearance and mild pericardial effusion. Coronary angiography excluded obstructive CAD and CMR confirmed diagnosis of recent myocarditis and worsening of left and right ventricular ejection fraction compared to a previous CMR. Patient was treated with evidence-based therapy for heart failure, prednisone, intravenous immunoglobulins, ibuprofen, and colchicine. Cardiac biomarkers reduced within the normal range, symptoms improved, and the patient was discharged asymptomatic and haemodynamically stable. Conclusions SARS-CoV-2, as already described in literature, can be associated with inflammatory cardiac involvement. This is the first report of SARS-CoV-2 associated myopericarditis in a patient with previous history of myocarditis and recent SARS-CoV-2 pneumonia. In our experience the patient was successfully treated with evidence-based therapy for heart failure and immunomodulation therapy.

Thrombotic risk in patients with COVID-19.

Emerging evidences prove that the ongoing pandemic of coronavirus disease 2019 (COVID-19) is strictly linked to coagulopathy even if pneumonia appears as the major clinical manifestation. The exact incidence of thromboembolic events is largely unknown, so that a relative significant number of studies have been performed in order to explore thrombotic risk in COVID-19 patients. Cytokine storm, mediated by pro-inflammatory interleukins, tumor necrosis factor α and elevated acute phase reactants, is primarily responsible for COVID-19-associated hypercoagulopathy. Also comorbidities, promoting endothelial dysfunction, contribute to a higher thromboembolic risk. In this review we aim to investigate epidemiology and clarify the pathophysiological pathways underlying hypercoagulability in COVID-19 patients, providing indications on the prevention of thromboembolic events in COVID-19. Furthermore we aim to reassume the pathophysiological paths involved in COVID-19 infection.

Cardiogenic Shock due to COVID-19-Related Myocarditis in a 19-Year-Old Autistic Patient.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is mainly responsible for respiratory involvement but cardiac complications are also reported. Nevertheless, potential life-threatening conditions in young people have not been described. A 19-year-old male autistic patient was admitted with fever and cough. The chest radiography showed viral pneumonia and the nasopharyngeal swab detected SARS-CoV-2. He rapidly developed hypotension, oliguria and increased myocardial injury markers and was treated with adrenaline, antiviral drugs and mechanical ventilation. Echocardiography revealed diffuse myocardial hypo-akinesia and decreased left ventricular ejection fraction (LVEF). After several days of treatment, the patient was weaned off mechanical ventilation, LVEF recovered to 50% and laboratory tests showed a decrease of markers of myocardial injury. Coronavirus disease 2019 (COVID-19) can therefore severely affect myocardium with life-threatening complications and even young people can be involved.

Unusual intracardiac thrombosis in two patients with coronavirus disease 2019 (COVID-19): case series.

BACKGROUND: COVID-19 may induce a coagulation dysregulation resulting in a prothrombotic state with a higher risk of arterial and venous thrombosis. This abnormal thrombotic diathesis can lead to pulmonary embolism, stroke, and intracardiac thrombosis. CASE SUMMARY: We present two cases of unusual intracardiac thrombosis in patients hospitalized for COVID-19. In both cases, imaging tests (such as transthoracic echocardiography (TTE), computed tomography scan of the chest, and cardiac magnetic resonance imaging) showed evidence of unusual intracardiac thrombosis with thrombi adherent to regularly contracting walls. DISCUSSION: This evidence confirms that COVID-19 induces a hypercoagulable state which can result in intracardiac thrombosis. Therefore, TTE is indicated in all COVID-19 patients for early diagnosis, and prompt anticoagulant therapy is to be considered as a thromboprophylaxis strategy.

Characteristics and outcomes of patients hospitalized for COVID-19 and cardiac disease in Northern Italy.

AIMS: To compare demographic characteristics, clinical presentation, and outcomes of patients with and without concomitant cardiac disease, hospitalized for COVID-19 in Brescia, Lombardy, Italy. METHODS AND RESULTS: The study population includes 99 consecutive patients with COVID-19 pneumonia admitted to our hospital between 4 March and 25 March 2020. Fifty-three patients with a history of cardiac disease were compared with 46 without cardiac disease. Among cardiac patients, 40% had a history of heart failure, 36% had atrial fibrillation, and 30% had coronary artery disease. Mean age was 67 ± 12 years, and 80 (81%) patients were males. No differences were found between cardiac and non-cardiac patients except for higher values of serum creatinine, N-terminal probrain natriuretic peptide, and high sensitivity troponin T in cardiac patients. During hospitalization, 26% patients died, 15% developed thrombo-embolic events, 19% had acute respiratory distress syndrome, and 6% had septic shock. Mortality was higher in patients with cardiac disease compared with the others (36% vs. 15%, log-rank P = 0.019; relative risk 2.35; 95% confidence interval 1.08-5.09). The rate of thrombo-embolic events and septic shock during the hospitalization was also higher in cardiac patients (23% vs. 6% and 11% vs. 0%, respectively). CONCLUSIONS: Hospitalized patients with concomitant cardiac disease and COVID-19 have an extremely poor prognosis compared with subjects without a history of cardiac disease, with higher mortality, thrombo-embolic events, and septic shock rates.

COVID-19 Pneumonia, Takotsubo Syndrome, and Left Ventricle Thrombi.

Left ventricle thrombus is considered a rare complication of Takotsubo syndrome. However, both a stress condition predisposing to Takotsubo syndrome and coagulation abnormalities coexist in COVID-19. We describe a case of a patient with COVID-19 with Takotsubo syndrome. (Level of Difficulty: Intermediate.).

Sinus Node Dysfunction in a Young Patient With COVID-19.

A 34-year-old man was admitted with acute lung injury and COVID-19 pneumonia. In the intensive care unit, he experienced episodes of prolonged asystole accompanied by hypotension without loss of consciousness. Once reversible causes were excluded, symptoms were related to dysfunction of the sinus node, and the patient underwent implantation of a pacemaker. (Level of Difficulty: Beginner.).