Cardiology

Packer, M. (2020). “Characterization, Pathogenesis, and Clinical Implications of Inflammation-Related Atrial Myopathy as an Important Cause of Atrial Fibrillation.” J Am Heart Assoc Apr 7;9(7):e015343. [Epub 2020 Apr 3].

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Historically, atrial fibrillation has been observed in clinical settings of prolonged hemodynamic stress, eg, hypertension and valvular heart disease. However, recently, the most prominent precedents to atrial fibrillation are metabolic diseases that are associated with adipose tissue inflammation (ie, obesity and diabetes mellitus) and systemic inflammatory disorders (ie, rheumatoid arthritis and psoriasis). These patients typically have little evidence of left ventricular hypertrophy or dilatation; instead, imaging reveals abnormalities of the structure or function of the atria, particularly the left atrium, indicative of an atrial myopathy. The left atrium is enlarged, fibrotic and noncompliant, potentially because the predisposing disorder leads to an expansion of epicardial adipose tissue, which transmits proinflammatory mediators to the underlying left atrium. The development of an atrial myopathy not only leads to atrial fibrillation, but also contributes to pulmonary venous hypertension and systemic thromboembolism. These mechanisms explain why disorders of systemic or adipose tissue inflammation are accompanied an increased risk of atrial fibrillation, abnormalities of left atrium geometry and an enhanced risk of stroke. The risk of stroke exceeds that predicted by conventional cardiovascular risk factors or thromboembolism risk scores used to guide the use of anticoagulation, but it is strongly linked to clinical evidence and biomarkers of systemic inflammation.

Mwipatayi, B. P., T. Anwari, J. Wong, E. Verhoeven, S. Dubenec, J. M. Heyligers, R. Milner, C. Mascoli, M. Gargiulo and W. P. Shutze (2020). “Sex-related outcomes after endovascular aneurysm repair within the Global Registry for Endovascular Aortic Treatment (GREAT).” Ann Vasc Surg Mar 16. pii: S0890-5096(20)30207-7. [Epub ahead of print].

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BACKGROUND: Abdominal aortic aneurysms (AAAs) are more common in men. However, women have been shown to have more short- and long-term adverse outcomes after endovascular aneurysm repair (EVAR). This disparity is thought to be multifactorial, including anatomical differences, hormonal differences, older age of presentation, and a greater degree of preoperative comorbidities. METHODS: A retrospective analysis that included data for 3758 patients from the Global Registry for Endovascular Aortic Treatment (GREAT) was conducted. Patients were recruited into GREAT between August 2010 and October 2016 and received the Gore Excluder stent graft for infrarenal AAAs repair. Cox multivariate regression analyses were performed to analyse any re-intervention and device related intervention rates. RESULTS: Of the 3758 patients, 3220 were male (mean age 73 years) and 538 were female (mean age 75 years). Women had higher prevalence rates of chronic obstructive pulmonary disease (P <0.0001) and renal insufficiency (P = 0.03), whilst men had higher rates of cardiovascular comorbidities. The AAAs in women were smaller in diameter with shorter and more angulated necks. Women did not experience a significantly higher rate of endoleaks, but did exhibit higher re-intervention rates, including re-intervention for device related issues. In terms of mortality, aorta related mortality was most prevalent within the first 30 days post procedure in both sexes. CONCLUSION: Women were treated at an older age and had a more hostile aneurysmal anatomy. Although the mortality rates were lower in women, they had significantly higher rates of re-intervention, and thus higher morbidity rates post EVAR.

McCullough, P. A., J. Eidt, J. Rangaswami, E. Lerma, J. Tumlin, K. Wheelan, N. Katz, N. E. Lepor, K. Vijay, S. Soman, B. Singh, S. P. McCullough, H. B. McCullough, A. Palazzuoli, G. M. Ruocco and C. Ronco (2020). “Urgent need for individual mobile phone and institutional reporting of at home, hospitalized, and intensive care unit cases of SARS-CoV-2 (COVID-19) infection.” Rev Cardiovasc Med 21(1): 1-7.

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Approximately 90 days of the SARS-CoV-2 (COVID-19) spreading originally from Wuhan, China, and across the globe has led to a widespread chain of events with imminent threats to the fragile relationship between community health and economic health. Despite near hourly reporting on this crisis, there has been no regular, updated, or accurate reporting of hospitalizations for COVID-19. It is known that many test-positive individuals may not develop symptoms or have a mild self-limited viral syndrome consisting of fever, malaise, dry cough, and constitutional symptoms. However some individuals develop a more fulminant syndrome including viral pneumonia, respiratory failure requiring oxygen, acute respiratory distress syndrome requiring mechanical ventilation, and in substantial fractions leading to death attributable to COVID-19. The pandemic is evolving in a clustered, non-inform fashion resulting in many hospitals with preparedness but few or no cases, and others that are completely overwhelmed. Thus, a considerable risk of spread when personal protection equipment becomes exhausted and a large fraction of mortality in those not offered mechanical ventilation are both attributable to a crisis due to maldistribution of resources. The pandemic is amenable to self-reporting through a mobile phone application that could obtain critical information on suspected cases and report on the results of self testing and actions taken. The only method to understand the clustering and the immediate hospital resource needs is mandatory, uniform, daily reporting of hospital censuses of COVID-19 cases admitted to hospital wards and intensive care units. Current reports of hospitalizations are delayed, uncertain, and wholly inadequate. This paper urges all the relevant stakeholders to take up self-reporting and reporting of hospitalizations of COVID-19 as an urgent task in combating this devastating pandemic.

Lo, K. B., P. A. McCullough and J. Rangaswami (2020). “Antihypertensive drugs and risk of COVID-19?” Lancet Respir Med(Mar 26. pii: S2213-2600(20)30156-9. [Epub ahead of print]).

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We caution against indiscriminate discontinuation of ACEIs and ARBs in patients who rely on these drugs for treatment of heart failure and who, additionally, might benefit from the postulated positive effects during overwhelming infection with SARS-CoV-2. Discontinuation of ACEIs or ARBs is associated with readmission to hospital and mortality among patients with heart failure.8 A surge of admissions to hospital for heart failure because of indiscriminate cessation of these important agents could overload already burdened health-care systems with vulnerable patients and cause diagnostic problems in view of the range of symptoms shared between acute heart failure and COVID-19, such as cough and shortness of breath. (Excerpt from text, no abstract available.)

Leeper, B. (2020). “Right Ventricular Failure.” AACN Adv Crit Care 31(1): 49-56.

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Interest in the right ventricle has increased because of advances in pulmonary hypertension treatment, improved diagnostic technology, and increased implantation of left ventricular assist devices and other mechanical circulatory assist devices. Right ventricular dysfunction is an independent predictor of mortality in patients with chronic heart failure. The purpose of this article is to describe the normal structure and function of the right ventricle, causes of right ventricular dysfunction leading to right ventricular failure, diagnostic hemodynamic assessments, and management of right ventricular failure in the critical care unit.