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MAY 08, 2020 — COVID-19, the disease caused by the novel coronavirus SARS-CoV-2, has produced morbidity and death in staggering numbers. At the time of this writing, COVID-19 is responsible for more than 210,000 deaths worldwide, including more than 56,000 deaths in the United States alone. By the time you read this, these numbers will have risen significantly.
The primary manifestation of COVID-19 is pulmonary in nature: fever with cough, dyspnea, and pneumonia. Now, anecdotal reports are suggesting that the virus also attacks the heart.
COVID-19: Is It Just the Lungs?
We’ve known that COVID-19 has profound pulmonary manifestations and can produce respiratory failure and acute respiratory distress syndrome. In recent months, however, we started hearing anecdotal reports from physicians in China and Italy about many of their patients who were not dying from pulmonary problems or hypoxemia. In fact, some would begin to show improvement from a pulmonary standpoint, but then, at around day 7 to 10 of symptoms, their condition would rapidly deteriorate because of deteriorating cardiac function.
We also heard reports that many of the critically ill patients never demonstrated radiographic signs of pneumonia, or that the radiographic findings did not correlate with the severity of the illness. Ruan and colleagues, Yang and colleagues, and Guo and colleagues, all in Wuhan, China, reported that many of the critically ill patients had elevated troponin (TN) levels, and that elevated levels of TN were correlated with prognosis. Based on this information, there’s been a tremendous amount of recent interest and investigation into the cardiac manifestations of COVID-19.
What Is Happening in the Heart?
The whole idea that severe viral infections, especially influenza-type infections, can cause cardiac problems is not new. In 2018, Kwong and colleagues described a 6-fold increased rate of acute myocardial infarction (AMI) during the first 7 days after diagnosis of influenza, with type B being significantly worse than type A (key point: Not all viruses are the same in this respect). In 2004, Madjid and Casscells reported that cardiovascular events were the most frequent cause of influenza-related death.
Viral infections produce a significant systemic inflammatory response, the degree of which varies with the specific virus; it appears that COVID-19 does produce significant systemic inflammation. Inflammation is a tremendous risk factor for inducing coronary plaque instability and rupture, which in turn can cause a type 1 AMI. These viral infections, especially coronavirus, also cause significant hypercoagulability, which is another predisposing factor leading to type 1 AMI. The result is that patients with COVID-19 are at increased risk for developing AMI due to acute coronary occlusion with ST-segment elevation (STE).
On the other hand, we’ve also been hearing reports of patients with STE on ECG who have no evidence of an acute coronary occlusion on coronary angiography. We’ve come to realize that COVID-19 can produce direct myocyte infection and injury with myocarditis with elevated TN levels and STE, and this can lead to decompensated heart failure and cardiogenic shock. The distinction between type 1 AMI with STE versus myocarditis with STE is extremely difficult purely based on the ECG results.
The treatment of these two conditions, however, is very different. Type 1 AMI is best managed with acute reperfusion therapy with primary percutaneous coronary intervention (PPCI) or fibrinolytics when PPCI is unavailable. By contrast, acute myocarditis requires aggressive hemodynamic supportive care.
How Do You Treat Patients With STE if COVID-19 Is a Concern?
In order to avoid exposing cardiac catheterization laboratory (CCL) personnel to coronavirus, some Chinese cardiologists recommended using fibrinolytic agents to treat patients with STE. Further justification for this practice was based on increasing reports that many patients with STE had negative coronary angiogram findings and were subsequently diagnosed with myocarditis.
Why send a patient with suspected myocarditis to the CCL? On the other hand, the use of fibrinolytics agents in a patient with myocarditis is not a safe treatment plan either, resulting in controversy regarding the best way to care for patients with STE.
In order to provide guidance to cardiologists and emergency physicians, the Society for Cardiovascular Angiography and Interventions, the American College of Cardiology, and the American College of Emergency Physicians have recently published a consensus statement on the management of acute myocardial infarction during the COVID-19 pandemic.
The statement reaffirms that PPCI is the standard of care for patients with presumed type 1 AMI, and that fibrinolytic agents should only be used if prompt PPCI cannot be performed. Fibrinolytic agents fail to establish successful reperfusion in nearly 50% of patients, and in these patients, rescue PCI is required, although with a greater risk of bleeding complications. This can be avoided if PPCI is chosen as first-line therapy.
In order to reduce the risk of exposure of healthcare workers to coronavirus, personnel should wear appropriate personal protective equipment when possible and not only when working with patients in whom there is a high suspicion of COVID-19.
The statement also acknowledges the possibility of myocarditis when patients have STE. If fibrinolytic agents are given to these patients for presumed type 1 AMI, these patients are subject to all the adverse effects of fibrinolytic agents without any benefits.
Furthermore, these patients will continue to demonstrate STE after receiving fibrinolytic agents, so they will require rescue PCI anyway before the definitive diagnosis of myocarditis can be made. If a patient’s medical history is inconsistent with type 1 AMI, the consensus statement recommends the use of early echocardiography to help diagnose type 1 AMI versus myocarditis.
Further details of the statement will be left to the reader. This document should be disseminated widely among emergency medicine and cardiology teams and will help provide a rational approach to managing these challenging patients.
In conclusion, here is a list of key points regarding COVID-19 and the heart:
COVID-19 is not purely a pulmonary disease. It produces multiorgan dysfunction, including cardiac dysfunction, which has been attributed as a common cause of death in infected patients.
Troponin levels predict cardiac involvement and prognosis of COVID-19.
Viral infections, particularly coronavirus, appear to induce systemic inflammation, which places patients at higher risk for type 1 acute myocardial infarction (AMI).
COVID-19 induces direct myocyte infection and injury with myocarditis, which can lead to decompensated heart failure and cardiogenic shock.
ST-segment elevation on ECG can be caused by type 1 AMI or myocarditis.
Primary percutaneous coronary intervention is the standard of care for patients with presumed type 1 AMI.
Patients with ST-segment elevation and an uncertain diagnosis should be assessed by echocardiogram or quickly be evaluated in the cardiac catheterization laboratory.
Amal Mattu, MD, is a professor, vice chair of education, and co-director of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland School of Medicine in Baltimore.