Prevalence of right ventricular dysfunction and impact on all-cause death in hospitalized patients with COVID-19: a systematic review and meta-analysis.

The Coronavirus Disease (COVID-19) pandemic imposed a high burden of morbidity and mortality. In COVID-19, direct lung parenchymal involvement and pulmonary microcirculation dysfunction may entail pulmonary hypertension (PH). PH and direct cardiac injury beget right ventricular dysfunction (RVD) occurrence, which has been frequently reported in COVID-19 patients; however, the prevalence of RVD and its impact on outcomes during COVID-19 are still unclear. This study aims to evaluate the prevalence of RVD and associated outcomes in patients with COVID-19, through a Systematic Review and Meta-Analysis. MEDLINE and EMBASE were systematically searched from inception to 15th July 2021. All studies reporting either the prevalence of RVD in COVID-19 patients or all-cause death according to RVD status were included. The pooled prevalence of RVD and Odds Ratio (OR) for all-cause death according to RVD status were computed and reported. Subgroup analysis and meta-regression were also performed. Among 29 studies (3813 patients) included, pooled prevalence of RVD was 20.4% (95% CI 17.1-24.3%; 95% PI 7.8-43.9%), with a high grade of heterogeneity. No significant differences were found across geographical locations, or according to the risk of bias. Severity of COVID-19 was associated with increased prevalence of RVD at meta-regression. The presence of RVD was found associated with an increased likelihood of all-cause death (OR 3.32, 95% CI 1.94-5.70). RVD was found in 1 out of 5 COVID-19 patients, and was associated with all-cause mortality. RVD may represent one crucial marker for prognostic stratification in COVID-19; further prospective and larger are needed to investigate specific management and therapeutic approach for these patients.

Right Ventricular Strain Is Common in Intubated COVID-19 Patients and Does Not Reflect Severity of Respiratory Illness.

BACKGROUND: Right ventricular (RV) dysfunction is common and associated with worse outcomes in patients with coronavirus disease 2019 (COVID-19). In non-COVID-19 acute respiratory distress syndrome, RV dysfunction develops due to pulmonary hypoxic vasoconstriction, inflammation, and alveolar overdistension or atelectasis. Although similar pathogenic mechanisms may induce RV dysfunction in COVID-19, other COVID-19-specific pathology, such as pulmonary endothelialitis, thrombosis, or myocarditis, may also affect RV function. We quantified RV dysfunction by echocardiographic strain analysis and investigated its correlation with disease severity, ventilatory parameters, biomarkers, and imaging findings in critically ill COVID-19 patients. METHODS: We determined RV free wall longitudinal strain (FWLS) in 32 patients receiving mechanical ventilation for COVID-19-associated respiratory failure. Demographics, comorbid conditions, ventilatory parameters, medications, and laboratory findings were extracted from the medical record. Chest imaging was assessed to determine the severity of lung disease and the presence of pulmonary embolism. RESULTS: Abnormal FWLS was present in 66% of mechanically ventilated COVID-19 patients and was associated with higher lung compliance (39.6 vs 29.4 mL/cmH2O, P = 0.016), lower airway plateau pressures (21 vs 24 cmH2O, P = 0.043), lower tidal volume ventilation (5.74 vs 6.17 cc/kg, P = 0.031), and reduced left ventricular function. FWLS correlated negatively with age (r = -0.414, P = 0.018) and with serum troponin (r = 0.402, P = 0.034). Patients with abnormal RV strain did not exhibit decreased oxygenation or increased disease severity based on inflammatory markers, vasopressor requirements, or chest imaging findings. CONCLUSIONS: RV dysfunction is common among critically ill COVID-19 patients and is not related to abnormal lung mechanics or ventilatory pressures. Instead, patients with abnormal FWLS had more favorable lung compliance. RV dysfunction may be secondary to diffuse intravascular micro- and macro-thrombosis or direct myocardial damage. TRIAL REGISTRATION: National Institutes of Health #NCT04306393. Registered 10 March 2020, https://clinicaltrials.gov/ct2/show/NCT04306393.

Echocardiographic Manifestations in COVID-19: A Review.

COVID-19 has rapidly spread around the world and threatened global health. Although this disease mainly affects the respiratory system, there is increasing evidence that SARS-CoV-2 also has effects on the cardiovascular system. Echocardiography is a valuable tool in the assessment of cardiovascular disease. It is cost-effective, widely available and provides information that can influence management. Given the risk of personnel infection and equipment contamination during echocardiography, leading world societies have recommended performing echocardiography only when a clinical benefit is likely, favouring focussed evaluations and using smaller portable equipment. In the past months, multiple reports have described a wide pattern of echocardiographic abnormalities in patients with COVID-19. This review summarises these findings and discusses the possible mechanisms involved.

Right ventricular load and contractility in HIV-associated pulmonary hypertension.

BACKGROUND: People living with human immunodeficiency virus (PLWH) are at risk of developing pulmonary hypertension (PH) and right ventricular (RV) dysfunction, but understanding of the relationship of RV function to afterload (RV-PA coupling) is limited. We evaluated the clinical and hemodynamic characteristics of human immunodeficiency virus (HIV)-associated PH. METHODS: We performed a retrospective review of patients with a diagnosis of HIV undergoing right heart catheterization (RHC) from 2000-2016 in a tertiary care center. Inclusion criteria were diagnosis of HIV, age ≥ 18 years and availability of RHC data. PH was classified as either pulmonary arterial hypertension (PAH; mean pulmonary arterial pressure [mPAP] ≥ 25mmHg with pulmonary artery wedge pressure [PAWP] ≤ 15mmHg) or pulmonary venous hypertension (PVH; mPAP ≥ 25mmHg with PAWP > 15). We collected demographics, CD4 cell count, HIV viral load, RHC and echocardiographic data. The single beat method was used to calculate RV-PA coupling from RHC. RESULTS: Sixty-two PLWH with a clinical likelihood for PH underwent RHC. Thirty-two (52%) met PH criteria (15 with PAH, 17 with PVH). Average time from diagnosis of HIV to diagnosis of PH was 11 years. Eleven of 15 individuals with PAH were on antiretroviral therapy (ART) while all 17 patients with PVH were on ART. Compared to PLWH without PH, those with PH had an increased likelihood of having a detectable HIV viral load and lower CD4 cell counts. PLWH with PAH or PVH had increased RV afterload with normal RV contractility, and preserved RV-PA coupling. CONCLUSION: PLWH with PH (PAH or PVH) were more likely to have a detectable HIV viral load and lower CD4 count at the time of RHC. PLWH with PAH or PVH had increased RV afterload, normal RV contractility, with preserved RV-PA coupling suggestive of an early onset, mild, and compensated form of PH. These results should be confirmed in larger studies.

COVID-19 infection in left ventricular assist device patients.

We describe two cases of favorable and unexpected recovery in positive patients with coronavirus disease 2019, suffering from multiorgan comorbidity and already assisted with the left ventricular assist device. We have observed that, although in the presence of more comorbidities, when the maintenance of a valid support of the cardiovascular function is guaranteed, the possibility of successfully overcoming the severe acute respiratory syndrome coronavirus 2 infection is still alive.

Mechanical circulatory support for cardiovascular complications in a young COVID-19 patient.

BACKGROUND: The current coronavirus (COVID-19) pandemic is associated with severe pulmonary and cardiovascular complications. CASE PRESENTATION: This report describes a young patient with COVID-19 without any comorbidity presenting with severe cardiovascular complications, manifesting with pulmonary embolism, embolic stroke, and right heart failure. CONCLUSION: Management with short-term mechanical circulatory support, including different cannulation strategies, resulted in a successful outcome despite his critical cardiovascular status.

Ultrastructural morphometric findings of cardiomyocytes in patients with impaired ventricular function--a comparative clinicopathological study.

AIM: The present study aims to analyze the differences in ultrastructural changes between right ventricular myocardium in clinically determined grades of heart failure (HF) [New York Heart Association (NYHA) classes I-IV] and their value in the routine diagnostic setting. METHODS: We investigated consecutive right ventricular endomyocardial biopsies of 12 patients presenting with HF (49±11.2years; male=10) by light microscopy and ultrastructural morphometric analysis. The patients were divided into four groups according to their NYHA classes (NYHA I: n=1, II: n=2, III: n=8, IV: n=1). We used a stereological point counting method on electron micrographs to determine the volume, surface, and numerical density of cardiomyocyte myofibrils; z-lines; mitochondria; and cristae as required. Further, secondary parameters were calculated. RESULTS: Myofibrillar parameters increased between NYHA class I and II (P<.01), which matched with more pronounced cardiomyocyte hypertrophy on the light microscopic level. In NYHA classes III and IV, the myofibrillar parameters dropped, while parameters concerning the mitochondria and their cristae rose (P<.01). This resulted in an elevated mitochondria to myofibril ratio (P<.05) and correlated with histologically evident atrophic cardiomyocytes, perinuclear loss of myofibrils and dot-like perinuclear staining positive on peroxide acid shift. CONCLUSION: In this present study, right ventricular myocardial ultrastructure differed between patients diagnosed with HF of different degrees in distinct subcellular changes. These findings suggest that ultrastructural analysis, while correlated with histopathological features, adds to the diagnosis in the routine diagnostic setting, specifically in lower NYHA grades, in which only minor changes are observed histologically.

Isolated right ventricular dysfunction in patients with human immunodeficiency virus.

BACKGROUND: HIV-infected individuals are at increased risk for pulmonary hypertension and cardiomyopathy, portending a poor prognosis. Right ventricular (RV) dysfunction is associated with worse outcomes in these conditions, yet its prevalence is poorly defined in HIV. We sought to determine the prevalence of RV dysfunction in an outpatient HIV cohort. METHODS: Echocardiograms were evaluated from 104 HIV-infected adults. Measurements included estimated pulmonary arterial systolic pressure (PASP) and several measures of RV function, including tricuspid annular plane systolic excursion (TAPSE), RV longitudinal myocardial strain (RVLMS), RV fractional area change (RVFAC), and myocardial performance index (MPI). RESULTS: Sixteen subjects (15%) had PASP >35 mm Hg, yet RV function did not differ significantly from those with normal estimated PASP. RV dysfunction defined by RVFAC <35% occurred in 11%. RVLMS had a median value of -27.3%, and individuals below the median had lower TAPSE but no differences in left ventricular ejection fraction (LVEF), PASP, or other measures. Dyspnea was associated with the lowest quintile of RVLMS (≥-21.05%). There were 6 subjects with LVEF <50%, and these individuals had lower TAPSE but no differences in PASP or other RV functional measures. CONCLUSIONS: RV dysfunction was common as estimated PASP >35 mm Hg and LV dysfunction, but these findings did not cosegregate. RV dysfunction in HIV-infected individuals may be a separate entity from LV/global cardiomyopathy or pulmonary hypertension and deserves further study.

Acute right ventricular myocarditis presenting with chest pain and syncope.

Myocarditis is assumed to involve both ventricles equally. Right ventricular predominant involvement is rarely described. A case of acute viral right ventricular myocarditis presenting with chest pain and syncope, grade 3 atrioventricular block, right ventricular dilatation and free wall hypokinesia is reported. Cardiac MRI showed late enhancement of the right ventricular free wall without involvement of the left ventricle. Anti-Coxsackie A9 virus neutralising IgM-type antibodies titre was elevated. This case emphasises that manifestations of myocarditis can be limited to the right ventricle and should be considered in the differential diagnosis of right ventricular enlargement.

Myocardial dysfunction during H1N1 influenza infection.

PURPOSE: The purpose of the study is to evaluate the incidence and hemodynamic consequences of right ventricular (RV) and left ventricular (LV) dysfunction in critically ill patients with H1N1 infection. PATIENTS AND METHODS: This is a retrospective analysis of all patients admitted to the intensive care unit of an academic hospital between October 2009 and March 2011 with severe H1N1 infection. Hemodynamic measurements and respiratory conditions were noted daily during the intensive care unit stay. RESULTS: Forty-six patients were admitted with severe H1N1 infection. Echocardiography was obtained in 39 patients on admission: 28 (72%) had abnormal ventricular function, of whom 13 (46%) had isolated LV abnormalities, 11 (39%) had isolated RV dysfunction, and 4 (14%) had biventricular dysfunction. Echocardiography was repeated in 19 of the 39 patients during their hospitalization: RV function tended to worsen with time, but LV function tended to normalize. The ventricular abnormalities were not associated with history, severity of the respiratory failure, or hemodynamic status. However, patients with ventricular dysfunction needed more aggressive therapy, including more frequent use of vasopressor and inotropic agents and of rescue ventilatory strategies, such as inhaled nitric oxide, prone positioning, and extracorporeal membrane oxygenation. CONCLUSIONS: These observations emphasize the high incidence of cardiac dysfunction in patients with H1N1 influenza infections.

Right and left cardiac function in HIV-infected patients investigated using radionuclide ventriculography and brain natriuretic peptide: a 5-year follow-up study.

OBJECTIVE: The aim of the study was to determine the incidence of myocardial dysfunction in an HIV-infected population receiving state-of-the-art treatment. METHODS: Between April 2001 and July 2002, 91 HIV-infected patients had a radionuclide ventriculography performed with determination of right ventricular ejection fraction (RVEF) and left ventricular ejection fraction (LVEF), as well as measurement of brain natriuretic peptide (BNP). Between July 2005 and January 2007, 63 patients (69%) agreed to participate in a follow-up study with a mean follow-up of 4.5 years. RESULTS: All patients had normal LVEF at both examinations. A minimal increase in mean LVEF of 0.02 was observed at follow-up (P=0.01). At the initial visit, four patients [6%; 95% confidence interval (CI) 2-15%] had a reduced RVEF, and at follow-up two patients (3%; 95% CI 0-11%) had slightly reduced RVEF. No significant change in mean RVEF was found. No patients had increased BNP and no change in mean plasma BNP was found. CONCLUSIONS: HIV-related cardiomyopathy appears not to constitute a problem in closely monitored, well-treated HIV-infected patients. Compared with pre-highly active antiretroviral therapy (HAART) studies, it seems that the improvement in immunocompetency and viral load has removed the problem of HIV-related cardiomyopathy. Although HAART has been suggested as a possible new cause of cardiomyopathy, we did not find any evidence of this.

Pathogenesis of HIV-associated heart disease.

As longevity increases in HIV-infected individuals after the introduction of highly active antiretroviral therapy regimens, long-term effects such as cardiovascular disease and, more specifically, symptomatic heart failure are emerging as leading health issues. In the present review article, we discuss HIV-associated cardiovascular disease, focusing on etiopathogenetic mechanisms that may play a role in diagnosis, management, and therapy of HIV-associated heart failure in the highly active antiretroviral therapy era.

Incidence of the involvement of the cardiovascular system in HIV infection.

The epidemiology of cardiac complications related to HIV, including cardiomyopathy, increased left ventricular mass, myocarditis, pericardial effusion, endocarditis, and malignancy, are discussed. An increased number of HIV-infected individuals may present with cardiac complications in the next decade as chronic viral infection, co-infections, drug therapy, and immunosuppression affect the heart. Understanding the nature and course of cardiac illness related to HIV infection may allow appropriate monitoring, early intervention and therapy, and will provide a baseline to evaluate the effects of new therapeutic regimens such as highly active antiretroviral therapy on the cardiovascular system.