Post-COVID Care Center to Address Rehabilitation Needs in COVID-19 Survivors: A Model of Care.

The severe acute respiratory syndrome coronavirus 2019 pandemic surge left a large cohort of patients vulnerable to cardiopulmonary, neurological, and psychiatric complications. This post-COVID Care center was established to identify patients with disease sequalae and deliver early multidisciplinary rehabilitation services. The evaluation included comprehensive history and physicals, screening tests, labs, and imaging to determine appropriate specialist referrals. After a 6-month period, 278 unique referrals were made to address symptoms reported by 114 patients in specialities including pulmonology, cardiology, and psychiatry. This framework allowed for individualized patient treatment and monitoring of disease after the acute phase of infection. This study highlights the substantial physical and psychosocial impact a coronavirus disease 2019 infection has on patients' long-term trajectory and emphasizes the need for early targeted rehabilitation Post-COVID Care centers. As the world transitions into the chronic phase of this pandemic, this model of care will provide a framework to improve the quality of health care delivery.

Corrected QT Interval Prolongation, Elevated Troponin, and Mortality in Hospitalized COVID-19 Patients.

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has risen to the level of a global pandemic. Growing evidence has proven the cardiac involvement in SARS-CoV-2 infection. This study aims to evaluate the ability of cardiovascular complications determined by elevated troponin and electrocardiogram findings (e.g., corrected QT interval (QTc)) in predicting the severity of SARS-CoV-2 infection among hospitalized patients. METHODS: This is a retrospective review of medical records of 800 patients, admitted to Richmond University Medical Center in Staten Island, NY, and tested positive for SARS-CoV-2 between March 1, 2020 and July 31, 2020. A total of 339 patients met the study inclusion and exclusion criteria and were included in statistical analysis. RESULTS: Elevated serum troponin levels on admission statistically correlated with mortality in SARS-CoV-2 patients. Prolonged QTc was shown to have an independent statistically significant association with mortality among patients hospitalized with SARS-CoV-2. CONCLUSIONS: Growing concern for cardiovascular sequelae of coronavirus disease 2019 (COVID-19) has prompted many researchers to investigate the role of cardiovascular complications in mortality due to SARS-CoV-2. Obtaining a simple electrocardiogram for hospitalized patients with COVID-19 could provide an independent prognostic tool and prompt more coordinated treatment strategies to prevent mortality among patients hospitalized with COVID-19.

Coronary Artery Ectasia: A Case Report Discussing the Causes, Diagnosis, and Treatment.

The localized or diffused dilation of a coronary artery lumen is referred to as coronary artery ectasia (CAE). Though it is well recognized, CAE is a rare finding that is encountered in the diagnostic procedure of coronary angiography. This form of atherosclerotic coronary artery disease (CAD) can be found in 1.4-4.9% of all coronary angiography patients. CAE can manifest in combination with stenotic lesions or present as an isolated condition. Its risk factors are similar to those of atherosclerosis. The underlying pathophysiology involves a vascular remodeling response to atherosclerosis. Enzymatic degradation by matrix metalloproteinases (MMP) and accumulation of lipoproteins play an important role in the remodeling process. CAE can be diagnosed with the help of imaging modalities such as coronary CT angiogram (CTA) and coronary magnetic resonance angiogram (MRA); coronary angiography is considered the gold standard procedure. The management strategies include treating the cardiovascular risk factors, prevention of thromboembolic events, and percutaneous/vascular revascularization. CAE can be managed medically, but percutaneous/surgical revascularization [coronary artery bypass grafting (CABG)] is an option to treat patients with co-existing symptomatic obstructive lesion refractory to medical treatment. Further trials are required to optimize the management guidelines related to CAE. In this report, we describe the case of a 42-year-old man with a past medical history of hypertension, hyperlipidemia, and asthma who presented with shortness of breath and minimally elevated troponin level. Coronary angiography revealed three vessels with ectasia and severe left ventricular dysfunction on ventriculography.

Atypical Myocardial Infarction with Apical Thrombus and Systemic Embolism: A Rare Presentation of Likely JAK2 V617F-Positive Myeloproliferative Neoplasm.

A few types of myeloproliferative neoplasms may be significant for Janus-associated kinase 2 mutation, JAK2 V617F, including polycythemia vera, essential thrombocythemia, and primary myelofibrosis. The prevalence of JAK2 mutation is low in the general population but higher in patients with myeloproliferative neoplasms. Some patients with JAK2 V617F-positive essential thrombocythemia are asymptomatic, but others may develop hemorrhagic or thromboembolic complications. Thromboembolism may occur in vessels of high flow organs like the heart and, thereby, present as myocardial infarction. Nonetheless, these patients are usually symptomatic with complaints of chest pain, for example. Atypical (asymptomatic) myocardial infarction with mild thrombocytosis may be the first clue for possible essential thrombocythemia with JAK2 V617F. In this report, we discuss a case of atypical (asymptomatic) myocardial infarction with secondary thromboembolism in a patient positive for JAK2 V617F with a likely myeloproliferative neoplasm.

Diagnosis and Management of 1:1 Atrial Flutter in the Setting of Aortic Valve Endocarditis and Embolic Stroke.

Atrial flutter is a rapid, regular atrial tachyarrhythmia that occurs most commonly in patients with underlying structural heart disease. Spontaneous 1:1 conduction of atrial flutter is indeed rare, but its diagnosis and management is of critical importance. We describe a case of a 65-year-old man with hypertension, preserved ejection fraction heart failure, end-stage renal disease, Parkinson's disease, and Alzheimer's dementia, in whom atrial flutter was associated with 1:1 atrioventricular conduction. Our patient was hemodynamically unstable with aortic valve endocarditis and recent septic embolic stroke. This case report emphasizes the importance of recognition and management to avoid hemodynamic compromise.

Endogenous Ouabain: An Old Cardiotonic Steroid as a New Biomarker of Heart Failure and a Predictor of Mortality after Cardiac Surgery.

Cardiovascular diseases remain the main cause of mortality and morbidity worldwide; primary prevention is a priority for physicians. Biomarkers are useful tools able to identify high-risk individuals, guide treatments, and determine prognosis. Our aim is to investigate Endogenous Ouabain (EO), an adrenal stress hormone with hemodynamic effects, as a valuable biomarker of heart failure. In a population of 845 patients undergoing elective cardiac surgery, we have investigated the relationships between EO and echocardiography parameters/plasmatic biomarker of cardiac function. EO was found to be correlated negatively with left ventricular EF (p = 0.001), positively with Cardiac End-Diastolic Diameter (p = 0.047), and positively with plasmatic NT-proBNP level (p = 0.02). Moreover, a different plasmatic EO level (both preoperative and postoperative) was found according to NYHA class (p = 0.013). All these results have been replicated on an independent cohort of patients (147 subjects from US). Finally, a higher EO level in the immediate postoperative time was indicative of a more severe cardiological condition and it was associated with increased perioperative mortality risk (p = 0.023 for 30-day morality). Our data suggest that preoperative and postoperative plasmatic EO level identifies patients with a more severe cardiovascular presentation at baseline. These patients have a higher risk of morbidity and mortality after cardiac surgery.

Association between erectile dysfunction and coronary artery disease. Role of coronary clinical presentation and extent of coronary vessels involvement: the COBRA trial.

AIMS: To investigate the prevalence of erectile dysfunction (ED) in patients with CAD according to clinical presentation, acute coronary syndrome (ACS) vs. chronic coronary syndrome (CCS), and extent of vessel involvement (single vs. multi-vessel disease). METHODS AND RESULTS: 285 patients with CAD divided into three age-matched groups: group 1 (G1, n=95), ACS and one-vessel disease (1-VD); group 2 (G2, n=95), ACS and 2,3-VD; group 3 (G3, n=95), chronic CS. Control group (C, n=95) was composed of patients with suspected CAD who were found to have entirely normal coronary arteries by angiography. Gensini's score used to assess extent of CAD. ED as any value <26 according to the International Index of Erectile Function (IIEF). ED prevalence was lower in G1 vs. G3 (22 vs. 65%, P<.0001) as a result of less atherosclerotic burden as expressed by Gensini's score [2 (0-6) vs. 40 (19-68), P=0.0001]. Controls had ED rate values similar to G1 (24%). Group 2 ED rate, IIEF, and Gensini's scores were significantly different from G1 [55%, P<0.0001; 24 (17-29), P=0.0001; 21 (12.5-32), P<0.0001] and similar to G3 suggesting that despite similar clinical presentation, ED in ACS differs according to the extent of CAD. No significant difference between groups was found in the number and type of conventional risk factors. Treatment with beta-blockers was more frequent in G3 vs. G1 and G2. In G3 patients who had ED, onset of sexual dysfunction occurred before CAD onset in 93%, with a mean time interval of 24 [12-36] months. In logistic regression analysis, age (OR=1.1; 95% confidence interval (CI), 1.05-1.16; P=<0.0001), multi-vessel vs. single-vessel (OR=2.53; 95% CI, 1.43-4.51; P=0.0002), and CCS vs. ACS (OR=2.32; 95% CI, 1.22-4.41; P=0.01) were independent predictors of ED. CONCLUSION: ED prevalence differs across subsets of patients with CAD and is related to coronary clinical presentation and extent of CAD. In patients with established CAD, ED comes before CAD in the majority by an average of 2 up to 3 years.

Cardiac stem cells possess growth factor-receptor systems that after activation regenerate the infarcted myocardium, improving ventricular function and long-term survival.

Cardiac stem cells and early committed cells (CSCs-ECCs) express c-Met and insulin-like growth factor-1 (IGF-1) receptors and synthesize and secrete the corresponding ligands, hepatocyte growth factor (HGF) and IGF-1. HGF mobilizes CSCs-ECCs and IGF-1 promotes their survival and proliferation. Therefore, HGF and IGF-1 were injected in the hearts of infarcted mice to favor, respectively, the translocation of CSCs-ECCs from the surrounding myocardium to the dead tissue and the viability and growth of these cells within the damaged area. To facilitate migration and homing of CSCs-ECCs to the infarct, a growth factor gradient was introduced between the site of storage of primitive cells in the atria and the region bordering the infarct. The newly-formed myocardium contained arterioles, capillaries, and functionally competent myocytes that with time increased in size, improving ventricular performance at healing and long thereafter. The volume of regenerated myocytes was 2200 microm3 at 16 days after treatment and reached 5100 microm3 at 4 months. In this interval, nearly 20% of myocytes reached the adult phenotype, varying in size from 10,000 to 20,000 microm3. Moreover, there were 43+/-13 arterioles and 155+/-48 capillaries/mm2 myocardium at 16 days, and 31+/-6 arterioles and 390+/-56 capillaries at 4 months. Myocardial regeneration induced increased survival and rescued animals with infarcts that were up to 86% of the ventricle, which are commonly fatal. In conclusion, the heart has an endogenous reserve of CSCs-ECCs that can be activated to reconstitute dead myocardium and recover cardiac function.

The artery size hypothesis: a macrovascular link between erectile dysfunction and coronary artery disease.

Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection satisfactory for sexual performance. Evidence is accumulating to consider ED as a vascular disorder. Common risk factors for atherosclerosis are frequently found in association with ED, and ED is frequently reported in vascular syndromes, such as coronary artery disease (CAD), hypertension, cerebrovascular disease, peripheral arterial disease, and diabetes mellitus. Finally, similar early impairment of endothelium-dependent vasodilatation and late obstructive vascular changes has been reported in both ED and other vascular syndromes. Recently, we proposed a pathophysiologic mechanism to explain the link between ED and CAD called the artery size hypothesis. Given the systemic nature of atherosclerosis, all major vascular beds should be affected to the same extent. However, symptoms rarely become evident at the same time. This difference in rate of occurrence of different symptoms is proposed to be caused by the different size of the arteries supplying different vascular beds that allow a larger vessel to better tolerate the same amount of plaque compared with a smaller one. According to this hypothesis, because penile arteries are smaller in diameter than coronary arteries, patients with ED will seldom have concomitant symptoms of CAD, whereas patients with CAD will frequently complain of ED. Available clinical evidence appears to support this hypothesis.

Common grounds for erectile dysfunction and coronary artery disease.

PURPOSE OF REVIEW: Evidence is accumulating to consider erectile dysfunction as a vascular problem. This review focuses on background, pathophysiological mechanisms and clinical evidence of the link between erectile dysfunction and coronary artery disease. RECENT FINDINGS: The link between erectile dysfunction and coronary artery disease is suggested by the following. (1) Common risk factors for atherosclerosis are frequently found in erectile dysfunction. (2) Erectile dysfunction is frequently found in vascular syndromes such as coronary artery disease, hypertension, cerebrovascular disease, peripheral arterial disease and diabetes. (3) A similar pathogenic involvement of the NO pathway leading to impairment of endothelium-dependent vasodilatation and late structural vascular abnormalities is shared by erectile dysfunction and vascular disorders. Given this background, the "artery-size hypothesis" is a recently proposed pathophysiological mechanism to explain the link between sexual dysfunction and myocardial ischemia. SUMMARY: Erectile dysfunction and coronary artery disease appear to be linked tightly each other.