Heart in Diabetes

Heart in Diabetes

Source:

Bozkurt B. COVID-19. Presented at: Heart in Diabetes Annual Meeting; Sept. 10-12, 2021 (hybrid meeting).

Disclosures: Bozkurt reports consulting for Amgen, Baxter, Bristol Myers Squibb, Relypsa, Sanofi Aventis and scPharmaceuticals, serving on the clinical event committee for a trial sponsored by Abbott and serving on the data safety monitoring committee for a trial sponsored by LivaNova.
September 10, 2021
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SARS-CoV-2 has multifaceted CV involvement, unlike previous coronaviruses

Source:

Bozkurt B. COVID-19. Presented at: Heart in Diabetes Annual Meeting; Sept. 10-12, 2021 (hybrid meeting).

Disclosures: Bozkurt reports consulting for Amgen, Baxter, Bristol Myers Squibb, Relypsa, Sanofi Aventis and scPharmaceuticals, serving on the clinical event committee for a trial sponsored by Abbott and serving on the data safety monitoring committee for a trial sponsored by LivaNova.
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In contrast to previous coronaviruses, SARS-CoV-2, the virus causing COVID-19, produces many CV consequences, according to a presentation at the Heart in Diabetes CME Conference.

“In the COVID-19 era, the spectrum of cardiovascular presentations ranged from acute coronary syndrome to heart failure to cardiogenic shock, most of which [had] a characterization of myocarditis-like presentation or acute inflammatory cardiomyopathy,” Biykem Bozkurt, MD, PhD, FHFSA, FACC, FAHA, FESC, Mary and Gordon Cain Chair and Professor of Medicine, director of the Winters Center for HF Research and associate director of the Cardiovascular Research Institute at Baylor College of Medicine, the W.A. “Tex” and Deborah Moncrief Jr., Chair and medicine chief at DeBakey VA Medical Center and immediate past president of the Heart Failure Society of America, said during her presentation. “The whole spectrum was so wide that we in the cardiovascular field were seeing cases ranging from presentations with arrhythmia to acute coronary syndrome to heart failure and cardiogenic shock to venous thromboembolism, and started recognizing that the underlying mechanism probably was multifactorial, and was hypothesized to be due to a variety of causes, such as cytokine storm, microvascular endothelial and thrombotic injury, hypoxemia and possibly direct infection of the cardiac myocytes.”

COVID-19
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Early reports showed evidence of myocardial injury in 25% to 30% of patients hospitalized for COVID-19, most commonly in patients with preexisting CVD, Bozkurt said, noting elevated levels of biomarkers of cardiac injury such as troponin were associated with mortality.

Biykem Bozkurt

Such elevated biomarkers were present in proportions ranging from 12% in those without known CVD to 46% in those who died from COVID-19 to 22% of those in the ICU, and were present in approximately 1% of patients with nonacute infection from previous coronaviruses, Bozkurt said.

Abnormal cardiac findings on echocardiography are common in patients hospitalized with COVID-19, particularly right ventricular dilatation or dysfunction, Bozkurt said.

COVID-19 has also been associated with elevated rates of out-of-hospital cardiac arrest and multisystem inflammatory syndrome, she said.

Among the post-acute sequelae of COVID-19 include heart palpitations and tachycardia, particularly postural orthostatic tachycardia, she said.

Cardiac MRI has detected cardiac abnormalities in many patients recovered from COVID-19, even in those who had mild disease, Bozkurt said.

“This created a lot of controversy about the safety of returning to sports in people who had COVID-19 infection,” she said, noting that rates in later studies with controls and rigorous diagnostic criteria were lower than in early studies without them.

A probable mechanism for all the CV complications from COVID-19 is that “SARS-CoV-2 can enter the cardiac myocytes — we know that from the ability to attach to the receptors, which is expressed in the cardiac myocytes through the ACE2-mediated entry,” Bozkurt said. “Initial case studies were supportive of acute viral myocarditis by lab echo findings, but not by histology. We also knew by measurements of RNA copies that SARS-CoV-2 was present inside the heart, but the histology does not show fulminant or lymphocytic myocarditis. The cardiac structure appears to be preserved [unlike] with other viral infections. SARS-CoV-2 can be identified in the interstitial cells or subendothelium, but not inside the cardiac myocytes, raising the possibility that it was present ... inside other circulating macrophages or in the interstitium. There is also evidence of microangiopathy and thrombosis in the setting of SARS-CoV-2 in the vasculature throughout the body. But the heart not showing myocarditis or confluent myocyte necrosis raises the question of how is the heart getting injured. The predominant feature appears to be macrophage.”

She said treatment recommendations include treating COVID-19 itself, treating all CV presentations of infection and treating all underlying CV conditions.