Cardiology

Roberts, W. C., S. Siddiquiz, A. E. Rafael-Yarihuaman and C. S. Roberts (2020). “Management of Adults With Normally Functioning Congenitally Bicuspid Aortic Valves and Dilated Ascending Aortas.” Am J Cardiol 125(1): 157-160.

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We describe herein a 65-year-old woman who underwent resection of a dilated (5.1 cm) ascending aorta associated with a normally functioning congenitally bicuspid aortic valve. The patient provided the framework to discuss proper management-operative versus nonoperative-of the dilated ascending aorta associated with a normally functioning bicuspid aortic valve. Unfortunately, there is inadequate data to provide an unequivocal answer to this dilemma. Operative intervention requires that the short-term risk of the prophylactic procedure be considerably lower than the long-term risk of aortic dissection/rupture without operative intervention. Because there is no proof that operative intervention provides less morbidity and lower mortality, nonoperative management at this time seems to be the better approach.

Roberts, C. S., Y. M. Salam, A. J. Moore and W. C. Roberts (2019). “Pseudoaneurysm of the Ascending Aorta at the Cannulation Site Diagnosed More Than Four Decades After Repair of Ventricular Septal Defect.” Am J Cardiol 124(12): 1962-1965.

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Described herein is a 69-year-old woman who developed a large saccular aortic aneurysm at a previous cannulation site for repair of a ventricular septal defect at age 25 years. The aneurysm was resected and proved histologically to be a false one. The long interval between operations (44 years) exceeds those reported previously.

Packer, M., C. S. P. Lam, L. H. Lund and M. M. Redfield (2020). “Interdependence of Atrial Fibrillation and Heart Failure With a Preserved Ejection Fraction Reflects a Common Underlying Atrial and Ventricular Myopathy.” Circulation 141(1): 4-6.

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Atrial fibrillation (AF) and heart failure with a preserved ejection fraction (HFpEF) are closely intertwined disorders that afflict millions of people, many of whom are obese or have diabetes mellitus or other proinflammatory conditions. Conceivably, the convergence of AF and HFpEF might be explained by 2 distinctly different frameworks. On the one hand, it is possible that each phenotype might lead sequentially to the other (ie, the increased left ventricular [LV] filling pressure in HFpEF may cause left atrial [LA] dilatation that triggers AF, and conversely, the rapid heart rate that accompanies AF might lead to LV fibrosis, although there is little evidence to support this hypothesis). On the other hand, and more likely, the 2 disorders may be parallel manifestations of the same underlying myocardial disease, which causes AF (because it affects the LA) and HFpEF (because it afflicts the LV) . . . AF and HFpEF demonstrate an exceptionally high degree of clinical and epidemiological convergence. Regardless of which disorder presents first, both are or will soon become evident in the same patients. AF and HFpEF appear to both be manifestations of a common underlying atrial and ventricular myopathy that is triggered when a systemic inflammatory or metabolic disorder causes coronary microvascular dysfunction and fibrosis of the atrial and ventricular myocardium, a process that may be mediated or exacerbated by inflammation in the adjoining epicardial adipose tissue. (Excerpts from text, p. 4-5; no abstract available.)

Packer, M. (2020). “Is Long-Standing Atrial Fibrillation a Biomarker of or Contributor to the Symptoms or Progression of Chronic Heart Failure?” Am J Med 133(1): 17-18.

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There is consensus that atrial fibrillation is a biomarker of the disease process in heart failure. Prolonged atrial distension due to chronic increases in left ventricular filling pressures contributes to the genesis of the arrhythmia. The disease process in the ventricles can also affect the atrial myocardium. Additionally, the atria are susceptible to fibrosis that results from the inflammation of epicardial adipose tissue that is seen in obesity or diabetes. The degree of atrial fibrosis is particularly marked in patients with persistent and long-standing atrial fibrillation. When the left atrium is severely fibrotic, restoration of sinus rhythm does not fully restore force transmission to the left ventricle. Patients with heart failure are at increased risk of stroke and systemic thromboembolism, whether in sinus rhythm or atrial fibrillation. The risk of stroke is higher in those with atrial fibrillation, perhaps because their atrial disease is more severe. Unless contraindicated, patients with atrial fibrillation should receive non-vitamin K-dependent oral anticoagulants, which have been shown to be noninferior or superior to warfarin in preventing stroke, but carry a lower risk of intracranial bleeding, particularly in patients with heart failure. However, even in sinus rhythm, the use of these drugs (e.g., rivaroxaban) in chronic heart failure appears to reduce the risk of stroke. Does atrial fibrillation itself contribute to the progression of heart failure? (Excerpt from text, p. 17; no abstract available.)

Packer, M. (2020). “HFpEF Is the Substrate for Stroke in Obesity and Diabetes Independent of Atrial Fibrillation.” JACC Heart Fail 8(1): 35-42.

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Both obesity and type 2 diabetes are important risk factors for the development of heart failure with a preserved ejection fraction (HFpEF), and both disorders increase the risk of systemic thromboembolic events. Traditionally, the risk of stroke has been explained by the strong association of these disorders with atrial fibrillation (AF). However, adiposity and diabetes are risk factors for systemic thromboembolism, even in the absence of AF, because both can lead to the development of an inflammatory and fibrotic atrial and ventricular myopathy, the 2 major elements of HFpEF. Atrial myopathy: 1) exacerbates pulmonary venous hypertension and exertional dyspnea; 2) leads to decreased flow, thrombogenesis, and systemic thromboembolization; and 3) often clinically manifests as AF; however, the relationship between AF and thromboembolism is unclear. Atrial fibrosis predisposes to thrombus formation, even in the absence of AF, and most thromboembolic events bear a poor temporal relationship to the occurrence of AF, whereas HFpEF (and the accompanying atrial disease) predicts stroke in patients with or without AF. Furthermore, rhythm control does not reduce the risk of stroke, although it reduces the burden of AF. These observations support the primacy of atrial myopathy as a critical component of HFpEF, rather than AF, as the mediator of systemic thromboembolism in obesity or diabetes. The well-established association between AF and stroke is likely explained by the fact that AF is a biomarker of more advanced inflammatory atrial disease but not necessarily a direct causal mechanism.