INTRODUCTION — Patients infected with the virus SARS-CoV-2 and its clinical disease COVID-19 are often minimally symptomatic or asymptomatic. More severe presentations include pneumonia and acute respiratory distress syndrome.
In some patients, the heart may be affected, and this can occur in individuals with or without a prior cardiovascular diagnosis. Evidence of myocardial injury, as defined as an elevated troponin level, is common among patients hospitalized with COVID-19, with putative causes including stress cardiomyopathy, hypoxic injury, ischemic injury (caused by cardiac microvascular damage or epicardial coronary artery disease), and systemic inflammatory response syndrome (cytokine storm). A minority of patients with an elevated troponin level present with symptoms and signs suggestive of an acute coronary syndrome. (See "COVID-19: Evaluation and management of cardiac disease in adults" and "Diagnosis of acute myocardial infarction", section on 'Clinical manifestations' and "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Clinical presentation' and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Clinical manifestations'.)
Patients with cardiovascular disease, hypertension, obesity, and diabetes are at increased risk of a poor prognosis. In addition, patients with myocardial injury, irrespective of cause, have a poorer prognosis.
This topic will address our approach to the diagnosis and management of patients with either an acute coronary syndrome or stable coronary artery disease (CAD) who are suspected of or who have confirmed COVID-19 infection. Our approach and recommendations only apply during the pandemic and are superseded by routine care thereafter.
The potential impact of the virus on the myocardium and conduction system is discussed elsewhere:
●(See "COVID-19: Evaluation and management of cardiac disease in adults".)
●(See "COVID-19: Arrhythmias and conduction system disease".)
The impacts of COVID-19 vaccines on the cardiovascular system are discussed elsewhere:
●(See "COVID-19: Vaccines", section on 'Specific safety concerns'.)
●(See "Myocarditis: Causes and pathogenesis", section on 'Vaccine-related'.)
●(See "COVID-19: Vaccine-induced immune thrombotic thrombocytopenia (VITT)".)
Other relevant topics include:
●(See "COVID-19: Epidemiology, virology, and prevention".)
●(See "COVID-19: Clinical features" and "COVID-19: Diagnosis".)
●(See "COVID-19: Management of the intubated adult".)
●(See "COVID-19: Management in hospitalized adults".)
●(See "Coronaviruses".)
EPIDEMIOLOGY — The prevalence of CAD in particular, and cardiovascular disease in general, varies from population to population. Thus, among patients who are diagnosed with COVID-19, there is a broad range for prevalent CAD. Rates between 4.2 and 25 percent have been reported, with most series from China [1-5]. Among patients admitted to intensive care units or those who died [5], the percent is higher.
The frequency of myocardial injury (as reflected by elevation in cardiac troponin levels) is variable among hospitalized patients with COVID-19, with reported frequencies of 7 to 28 percent. (See "COVID-19: Cardiac manifestations in adults", section on 'Troponin'.)
Decline in hospitalization and percutaneous coronary intervention rates — Multiple studies have found that the incidence of hospitalization for acute myocardial infarction (MI) and admissions for most diagnoses have decreased by as much as 40 to 50 percent during the pandemic [6-13]. The following three large studies are representative:
●A study from Northern California compared weekly incidence rates of hospitalization for acute MI (ST-elevation MI [STEMI] and non-ST-elevation MI [NSTEMI]) before and after March 4, 2020, when the first reported death from COVID-19 occurred in Northern California [8]. These data were also compared with data from the same time period in 2019. The weekly rates of hospitalization decreased by about 48 percent during the COVID-19 period (during the period of January 1 to March 3, 2020, the incidence rate was 4.1 per 100,000 person-weeks and from April 8 to April 14, the incidence rate was 2.1 per 100,000 person-weeks [incidence rate ratio 0.52, 95% CI 0.40-0.68]). This decrease occurred in patients with NSTEMI (incidence rate ratio 0.51, 95% CI 0.38-0.68) and probably in patients with STEMI (incidence rate ratio 0.60, 95% CI 0.33-1.08). Compared with 2019, the incidence of hospitalization for acute MI was significantly lower in 2020 only after March 4, demonstrating that the decrease could not be explained by seasonal variation.
●A study from Italy compared admissions for acute MI to coronary care units from March 12 to 19 in 2020 with those during the equivalent week in 2019 [9]. There was a 49.4 percent reduction (p<0.001 percent), and the reduction was significant for both STEMI and NSTEMI. The STEMI case fatality rate was higher, comparing 2020 with 2019 (risk ratio 3.3, 95% CI 1.7-6.6).
●A large database study from England compared hospital admissions for acute coronary syndromes (ACS) between mid-February and end of March, 2020 and also compared them with the weekly average in 2019 (3017 per week) [11]. There was a substantial reduction in the weekly numbers of patients with ACS admitted to hospitals in England by the end of March, 2020 (1813 per week; 40 percent reduction) compared with the 2019 weekly average. The trend was partially reversed by the end of May, 2020 (2522 per week; 16 percent reduction). Although the decline in hospital admissions was seen across all types of ACS (eg, STEMI, NSTEMI, unstable angina, and MI of unknown type), it was most pronounced for those with NSTEMI.
Possible explanations for the decreased hospitalization rate include patient fear of being infected if hospitalized (avoidance of medical care) and a redistribution of health care.
Perhaps consequent to the decrease in hospitalization rates, at least three studies have documented a decline in the number of acute coronary syndrome patients referred for percutaneous coronary intervention [11,13,14].
IMPACT ON THE CARDIOVASCULAR SYSTEM — It is likely that COVID-19 directly and indirectly affects the cardiovascular system. Potential mechanisms of cardiovascular injury include direct myocardial injury from hemodynamic derangement or hypoxemia, inflammatory myocarditis, stress cardiomyopathy, microvascular dysfunction or thrombosis due to hypercoagulability, or systemic inflammation (cytokine storm), which may destabilize coronary artery plaques [15].
Studies suggest that COVID-19 increases the risk of acute MI [16-18]. In one study, there was an increased risk of acute MI in patients with a new diagnosis of COVID-19 compared to noninfected controls (0.03 versus 0.01 percent; adjusted odds ratio 1.22, 95% CI 1.08-1.38) [19].
The clinical impact of SARS-CoV-2 infection is greater in those with prior cardiovascular disease (CVD) and increasing age. In one study, patients with prior CVD made up 22.7 percent of all fatal cases, and the case fatality rate was 10.5 percent [20].
COVID-19 vaccination can cause cardiovascular disease (eg, pericarditis, myocarditis). A more detailed discussion of the cardiovascular effects of COVID-19 vaccines is presented elsewhere. (See "COVID-19: Vaccines", section on 'Specific safety concerns' and "Myocarditis: Causes and pathogenesis", section on 'Vaccine-related'.)
ASSOCIATION BETWEEN BASELINE CVD AND COVID-19 — There is substantial evidence of an association between cardiovascular disease (CVD) risk factors of hypertension, diabetes, prior CAD, and the risk and severity of COVID-19 infection (table 1) [2,3,21-24]. (See "COVID-19: Clinical features", section on 'Risk factors for severe illness'.)
The following two observational studies illustrate the magnitude of the relationship:
●In a report from the Chinese Center for Disease Control and Prevention, 72,314 cases (44,672 confirmed) reported by February 11, 2020 were reviewed [25]. The crude mortality rate was 2.3 percent. For age over 80, the case fatality rate was 14.8 percent. History of coronary heart disease (CHD) was present in 4.2 percent of all cases, but in 22.7 percent of fatal cases. Case fatality rates were 10.5 percent for CHD, 7.3 percent for diabetes, and 6 percent for hypertension. Another report evaluated 1099 cases from 30 provinces within mainland China [24]. Of these, 15.7 percent were classified as severe, and 6.1 percent had a primary endpoint, defined as intensive care unit admission, mechanical ventilation, or death. The presence of diabetes (severe versus nonsevere disease, 16.2 versus 5.7 percent; primary endpoint versus no primary endpoint, 26.9 versus 6.1 percent), hypertension (23.7 versus 13.4 percent; 35.8 versus 13.7 percent), or CHD (5.8 versus 1.8 percent; 9 versus 2 percent) was significantly more frequent among patients with severe disease versus nonsevere disease and with a primary endpoint versus no primary endpoint. In a report of 191 patients from Wuhan province who were diagnosed before January 31, 2020, there were significant univariate associations with death outcome for diabetes (31 versus 14 percent, p = 0.005), hypertension (48 versus 23 percent, p = 0.0008), and CHD (24 versus 1 percent, p<0.0001) [3]. In a multivariable analysis, only advancing age, Sequential Organ Failure Assessment Score, and D-Dimer were associated with mortality.
●Another study found that the presence of acute injury determined by troponin elevation was a significant factor in the association of CVD and mortality [26] (see 'Troponin' below). Among 187 patients with confirmed COVID-19, a history of CVD (defined as CHD, hypertension, or cardiomyopathy) was present in 66 (35 percent), and troponin was elevated in 52 (28 percent). Troponin elevation was more frequent in patients with CVD (55 percent, 36 of 66). Among patients with CVD and elevated troponin, the mortality rate was 69 percent (25 of 36). The mortality rate was 7.6 percent among patients without CVD and normal troponin, 13.3 percent among those with CVD and normal troponin, 37.5 percent among those without CVD and elevated troponin, and 69.4 percent among those with CVD and elevated troponin. Furthermore, troponin elevation correlated with elevations in C-reactive protein, and higher troponin elevations predicted higher mortality. Although the number of patients included limits the interpretation, there is a suggestion that patients with underlying CVD (including hypertension) are both at increased risk for acute injury and worsened survival in the setting of injury. The cause of this association and whether injury indicates increased risk for MI or myocarditis will require additional investigation.
Until more data with larger numbers of patients are available, it seems reasonable to consider all patients with history of CVD, hypertension, or diabetes at higher risk. We consider this risk likely to be highest for patients with these risk factors, older age, known history of heart failure, or clinically significant valvular disease. For now, there are no specific measures based on this risk stratification, but we advise all of our patients with these risk factors to be especially cautious regarding public health measures of social distancing, including with close family members. Furthermore, given the association with more severe disease and increased risk for acute myocardial injury, we advise early clinical evaluation for any suspect symptoms.
ACUTE CORONARY SYNDROME PATIENTS
Definitions — The term acute coronary syndrome (ACS) is applied to patients in whom there is a suspicion or confirmation of myocardial injury. ACS patients may have either STEMI or non-ST-elevation ACS, which includes NSTEMI or unstable angina. According to the Fourth Universal Definition of MI (see "Diagnosis of acute myocardial infarction", section on 'Definitions'), the term acute MI should be used when there is acute myocardial injury with clinical evidence of acute myocardial ischemia and with detection of a rise and/or fall of cardiac troponin values with at least one value above the 99th percentile upper reference limit and at least one of the following [27]:
●Symptoms of myocardial ischemia.
●New ischemic ECG changes. (See 'Diagnosis and differential diagnosis' below.)
●Development of pathological Q waves.
●Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.
●Identification of a coronary thrombus by angiography or autopsy (not for type 2 or 3 MI).
The Fourth Universal Definition of MI includes a clinical classification according to the assumed proximate cause of the myocardial ischemia:
●Type 1 – MI caused by acute atherothrombotic CAD and usually precipitated by atherosclerotic plaque disruption (rupture or erosion).
●Type 2 – MI consequent to a mismatch between oxygen supply and demand.
With COVID-19 infection, the majority of MIs are type 2 and related to the primary infection, hemodynamic, and respiratory derangement. As such, the primary disorders should be treated, and in most cases the patient can be treated conservatively with regard to coronary disease. If a type 1 infarction is thought to be the primary etiology of the MI, standard therapies can be considered. (See "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Overview of the acute management of ST-elevation myocardial infarction".)
Clinical manifestations — The vast majority of patients presenting with a systemic illness consistent with COVID-19 will not have symptoms or signs of CAD. Patients may be tachycardic (with or without palpitations) in the setting of other illness-related symptoms.
In patients with COVID-19, the clinical manifestations of acute CAD are likely similar to those without the virus. (See "Diagnosis of acute myocardial infarction", section on 'Clinical manifestations'.)
Few patients hospitalized with COVID-19 have complained of chest pain on admission, but the true prevalence and characteristics of chest pain among COVID-19 patients are unknown [1,28].
Physicians report that there are fewer ACS patients presenting to the hospital during the pandemic (see 'Epidemiology' above). In addition, there is concern that patients with ACS are presenting later to emergency departments or not coming at all due to fear of exposure to patients with COVID-19. These patients will suffer unnecessary morbidity and mortality without proper ACS management. Health care providers should make every effort to persuade patients with complaints suggestive of ACS to seek proper evaluation while ensuring that appropriate screening and protection are available to avoid patient and provider concerns regarding nosocomial spread of the infection. If admitted, it is prudent to screen all patients for symptoms of COVID-19 (eg, fever, cough, dyspnea, sore throat, gastrointestinal disturbance) regardless of the primary complaint. (See "COVID-19: Clinical features", section on 'Clinical manifestations'.)
The pandemic varies in terms of intensity between regions. There are epicenters with extreme COVID-19-associated disease burden, whereas other areas continue to see more regular ACS and only rarely COVID-19 patients.
Assessment of COVID-19 status — ACS patients with unknown COVID-19 status are treated as potential COVID-19 patients since aerosolization during intubation or cardiopulmonary resuscitation in the catheterization laboratory is possible.
Testing for COVID-19 is recommended for NSTEMI patients who are stable prior to transfer for catheterization.
ST-elevation myocardial infarction — Irrespective of COVID-19 status, urgent or emergent diagnosis and treatment are essential to improve outcomes in patients with STEMI. Patients calling the health care system with ischemic-type chest pain or anginal equivalent should be urged to present to an emergency department. (See 'Acute coronary syndrome patients' above.)
Patient and health care system factors have led to delays in the presentation of patients with STEMI. Later presentation has likely led to worse outcomes [29]. In addition, reperfusion delays by as much as 20 minutes have been reported [12].
There have been reports of increased coronary artery thrombus burden in patients with STEMI [29]. This is consistent with an increased frequency of thrombotic strokes, particularly in young people, during the pandemic. Alterations in the coagulation system, abnormal platelet function, or abnormal endothelial function have been postulated [30]. (See "COVID-19: Hypercoagulability".)
Our approach to ST-elevation myocardial infarction — Our approach, which is summarized below, is generally in agreement with a provided algorithm (algorithm 1). The only way in which we differ slightly from the algorithm is that if we think STEMI with an occluded vessel is more likely than not, and that the benefit of a confirmed open artery is likely to impact overall recovery, we favor primary percutaneous coronary intervention (PCI).
The following bullets summarize information contained in the next two sections. (See 'Diagnosis and differential diagnosis' below and 'Management' below.)
For COVID-19 patients or those under investigation [31]:
●In patients who are critically ill due to COVID-19 infection (eg, acute respiratory distress syndrome or multiorgan failure), the decision to reperfuse (with either primary PCI or fibrinolysis) or not should be managed on a case-by-case basis.
●If the patient is not critically ill, we attempt reperfusion, and we perform primary PCI rather than fibrinolysis in most cases, similar to patients without COVID-19. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy", section on 'Primary PCI preferred to fibrinolysis'.)
In some circumstances, available local resources and the ability to protect the staff from infection also need to be taken into account. Some centers have chosen to administer fibrinolytic therapy in eligible patients [29].
●Irrespective of COVID-19 status, we mask all patients and we use personal protective equipment for all staff.
Diagnosis and differential diagnosis — However, during the pandemic, alternative causes of myocardial injury (such as stress [Takotsubo] cardiomyopathy or myocarditis) are important to consider (table 2).
STEMI usually requires that the patient have chest pain or anginal equivalent symptomatology and ECG characteristics that include ST-segment elevation in at least two contiguous leads (see "Diagnosis of acute myocardial infarction", section on 'ST elevation'):
●New ST-segment elevation at the J-point in two contiguous leads with the cut-points: ≥0.1 mV in all leads other than leads V2 to V3.
●For leads V2 to V3: ≥2 mm in men ≥40 years of age, ≥2.5 mm in men <40 years of age, or ≥1.5 mm in women regardless of age.
●In the absence of ST elevation on ECG, new left bundle branch block with anginal symptoms is considered to be a STEMI equivalent.
However, ECG criteria are not specific for coronary artery thrombosis, particularly in COVID-19 patients in whom ST elevation may occur with stress cardiomyopathy or possibly myocarditis. Thus, noncoronary artery COVID-19-associated myocardial injury needs to be carefully considered as a diagnostic possibility before reperfusion therapy is considered. In most patients with ST elevation, the diagnosis will be thrombotic occlusion of a coronary artery. (See "COVID-19: Evaluation and management of cardiac disease in adults".)
For patients with an elevated troponin and suspected STEMI, echocardiography is not generally used to identify which patients need emergent angiography since we believe the vast majority of patients require angiography regardless of echocardiographic findings. (See 'Echocardiography' below.)
Management — For STEMI patients who are known to not be infected with the virus, we manage them with the usual approach of primary PCI except that we mask all patients. If myocarditis seems more likely than STEMI (see 'Diagnosis and differential diagnosis' above), we suggest a conservative approach with aspirin and heparin administration until the diagnosis becomes clearer.
For confirmed cases or COVID-19 status under investigation in patients with STEMI, there are two important early management questions:
●Does the patient have a life-threatening (critical) illness, such as respiratory failure from COVID-19, that makes them a less-than-ideal candidate for reperfusion? Practitioners typically asked this question before revascularization in all patients prior to the pandemic. During the pandemic, it is an essential question.
●During the pandemic, should fibrinolytic therapy be used more liberally as the choice for early reperfusion?
With regard to the first issue, the harm associated with pursuing reperfusion therapy may exceed the anticipated gain in some COVID-19 patients, particularly if the primary competing illness portends a poor outcome. As is true for all patients with STEMI, comorbidities, size of infarction, delay to presentation, and hemodynamic status must be considered when determining if reperfusion therapy will be employed.
Regarding the second issue, and with the understanding that PCI is generally preferred to fibrinolytic therapy, some experts have raised the possibility that a more liberal use of fibrinolytic therapy (than what is normally recommended) may be necessary in some settings due to resource utilization and risk of viral exposure for health care providers. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy", section on 'Summary and recommendations'.)
The argument, in part, is that there will be less viral exposure to the catheterization laboratory staff. It should be recognized, however, that fibrinolysis may not reduce resource utilization during the pandemic since the majority of patients receiving fibrinolytic therapy will still require coronary angiography at some point during hospitalization, usually within 3 to 24 hours as part of a pharmacoinvasive or rescue strategy for fibrinolysis failure (see "Percutaneous coronary intervention after fibrinolysis for acute ST-elevation myocardial infarction"). These patients will require monitoring in an intensive care unit, thereby utilizing a scarce resource and prolonging length of stay. Furthermore, there are some patients who may be exposed to the risk of bleeding from fibrinolysis, specifically intracranial hemorrhage, in the setting of myocarditis, and some may not realize the benefit of myocardial salvage in the context of a competing life-threatening illness or small territory at risk. As such, we continue to prefer PCI as the reperfusion strategy during the COVID-19 pandemic. Nevertheless, the decision must be considered in the larger context of the availability of resources within the system, as well as important patient factors including age, infarct location, and duration of symptoms that influence fibrinolysis efficacy, bleeding risk, and the chances of substantial myocardial salvage.
When deciding between primary PCI and fibrinolytic therapy, factors such as significant associated comorbidities and hospital resource limitations should be taken into account. For example, a patient with COVID-19 pneumonia with respiratory failure may not be an optimal candidate to reap the benefit of myocardial reperfusion, while a patient with suspected COVID-19 and mild or moderate infection is likely to benefit from myocardial salvage, and if the resources are available, then reperfusion should be performed despite the risk to providers and the resources required.
Irrespective of the initial reperfusion strategy, we treat all STEMI patients with early aspirin, P2Y12 inhibitor, and anticoagulation. High-dose statin is started as soon as possible after the diagnosis.
Outcomes in COVID-19 patients — In patients with STEMI and concomitant COVID-19, the risk of mortality is higher when compared with patients with STEMI who do not have COVID-19. This increased risk is likely related to the mortality directly associated with COVID-19 and to the inability to provide appropriate STEMI management to all patients with COVID-19. (See 'Management' above.)
A large administrative claims database was used to assess the effects of COVID-19 among 76,434 patients with out-of-hospital STEMI (present on admission) and 4015 patients with in-hospital STEMI (recorded after hospital admission) [32]. Among the patients with out-of-hospital STEMI, coronary angiography and primary PCI were used with similar frequency in those with and without COVID-19 (approximately 82 and 70 percent, respectively), but patients with COVID-19 had a higher risk of in-hospital mortality (15 versus 11 percent; adjusted odds ratio [OR] 1.4, 95% CI 1.1-1.9). Among the patients who had an in-hospital STEMI with or without associated COVID-19, those with COVID-19 were less likely to undergo coronary angiography (35 versus 45 percent) or receive primary PCI (1 versus 9 percent) and had a higher risk of in-hospital mortality (77 versus 44 percent; adjusted OR 4.1, 95% CI 3.0-5.7).
Non-ST-elevation myocardial infarction — NSTEMI patients require urgent management but generally do not require a catheterization laboratory emergently (see "Non-ST-elevation acute coronary syndromes: Revascularization", section on 'Timing'). In the face of resource limitation during the COVID-19 pandemic, any decision to proceed with an invasive strategy should take into account current health care resources. In some geographies, cardiac catheterization laboratories have been converted to intensive care units.
For patients in whom medical therapy is likely to lead to a worse outcome (ie, higher-risk patients) (see "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Very high-risk patients' and "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Early risk stratification tools'), we attempt to utilize the catheterization laboratory.
We perform urgent catheterization on NSTEMI patients for reasons such as ongoing evidence of myocardial ischemia (eg, repetitive episodes of angina or dynamic ECG changes, ventricular arrhythmias, or heart failure).
Other complications have included arrhythmias and shock. In one study, these were reported in 17, 7, and 9 percent of patients, respectively [1]. In a series of 21 severely ill patients admitted to the intensive care unit in the United States, one-third developed cardiomyopathy [33].
Diagnosis uncertain — Where there is uncertainty as to whether the individual has an ACS due to plaque rupture, combined use of clinical evaluation and ECG is usually sufficient to make a decision. (See "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome" and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".)
Consultation with a cardiologist is suggested for cases where the diagnosis remains uncertain.
Echocardiography — Among patients with COVID-19 with suspected ACS, the role of echocardiography in altering the pretest probability of CAD is limited to low- or intermediate-risk patients. In patients with COVID-19, an echocardiogram may be performed if requested by a consulting cardiologist and if it is expected to have a significant impact on management or is likely to change the patient's prognosis. (See "Noninvasive testing and imaging for diagnosis in patients at low to intermediate risk for acute coronary syndrome" and "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome".)
Findings on an echocardiogram that favor a condition other than ACS (eg, stress cardiomyopathy, myocarditis, pericarditis, or noncardiac cause of chest pain) include:
●No wall motion abnormalities during chest pain
●Wall motion abnormalities not supportive of regional injury suggested by the ECG
●Wall motion abnormalities in a noncoronary distribution
●Less specific findings, such as small pericardial effusion
It is recognized that focal wall motion abnormalities may be present in patients with noncoronary myocardial injury and conversely that global dysfunction may accompany ACS, and so the echocardiography cannot be the sole determinant of whether reperfusion therapy is pursued.
The role of echocardiography in patients with COVID-19 without suspected ACS is discussed separately. (See "COVID-19: Evaluation and management of cardiac disease in adults".)
Cardiogenic shock — The primary disorder in the majority of patients with severe COVID-19 infection is hypoxia-related respiratory failure. A proportion develop systemic hyperinflammatory response and vasodilatory shock as the viremia clears. This phase of illness may be accompanied by concomitant myocardial suppression and cardiogenic shock. This mixed etiology of shock can be difficult to manage, particularly if the patient has preexisting cardiovascular dysfunction. It has been observed infrequently that more severe cardiovascular dysfunction occurs with mild respiratory compromise and inflammation. It is possible that these patients are suffering from myocardial injury as a manifestation of or response to the infection [34]. (See "COVID-19: Evaluation and management of cardiac disease in adults" and "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Systemic inflammatory response syndrome (SIRS)' and "COVID-19: Management of the intubated adult".)
There are anecdotal reports of patients recovering from the respiratory illness with subsequent abrupt cardiovascular collapse. Whether this is related to an inflammatory or some other process remains uncertain. It remains to be described whether an unchecked inflammatory response results in these late hemodynamic sequelae.
Other issues
Issues facing catheterization laboratory personnel — We generally agree with approaches outlined in a report from the American College of Cardiology's Interventional Council and the Society of Cardiovascular Angiography and Intervention [35]. Similar protocols have been created, including one from the Interventional Cardiology Association and Heart Rhythm Association of the Spanish Society of Cardiology [36].
Efforts should be made to avoid the patient remaining in waiting areas and halls, particularly in which staff will be directly interacting with the patient. Equipment for PCI (eg, sheath, guiding catheter, and possibly a workhorse wire and balloon) should be placed in the room prior to patient arrival to avoid repeated entry and exit of the staff.
We encourage training and simulation in donning and doffing personal protective equipment (PPE), observing to monitor adherence to best practices, and reading the proper sequences (figure 1 and figure 2) [37] (see 'Donning and doffing personal protective equipment' below). We recommend daily checks to ensure adequate PPE is available and standard checks of the "code" or "crash" cart. There is no consensus as to whether positive-pressure catheterization rooms should be converted to no-pressure or negative-pressure rooms.
If resources allow, it appears prudent to designate one room for suspected/confirmed COVID-19-positive patients, recognizing this may not be possible in some situations. Equipment in closed cabinets is not thought to require disinfectant after a procedure that involves a patient with established or suspected COVID-19, but only a minimal amount of supplies and equipment should be kept in this room. Unused equipment that is not covered, especially if the procedure involved aerosolization (eg, intubation, transesophageal echocardiography, cardiopulmonary resuscitation [CPR]), should be discarded or the packaging should be disinfected before additional use. The minimal number of personnel should enter the room, with at least the operator or a nurse in the room and a technologist in the control booth.
Donning and doffing personal protective equipment — A reasonable sequence for donning and doffing PPE is as follows (see "COVID-19: Infection prevention for persons with SARS-CoV-2 infection"):
●Remove any personal items.
●Put on the lead apron.
●Put on a disposable gown.
●Gather the necessary PPE and check for its integrity.
●Perform hand hygiene with alcohol hand gel/rub.
●Put on the proper disposable respirator (N95 or FFP2 standard; FFP3 is available for anesthesiologists and nurses helping with airway maneuvers).
●Put on hair cover.
●Put on shoe covers.
●Put on goggles and/or face shield, avoiding any interference with the respirator.
●Perform hand hygiene.
●Put on the first pair of gloves.
●Put on a second gown (sterile or not, according to your role in catheterization laboratory), not using the inside tie.
●Put on a second pair of gloves (over cuff) (sterile if needed).
A safe doffing area should be identified in each catheterization laboratory, in particular if no anteroom exists. If no anteroom is available, doffing of PPE could be done inside the laboratory, at the end of procedure, and when the patient has been transferred away. Only the facial respirator must be removed outside the contaminated area. The following are sequential steps:
●Avoid any contact with your face, hair, and eyes before completing the entire doffing process.
●Place any disposable PPE in the clinical waste bin.
●Do not fill the clinical waste bin more than three-fourths full in order to be able to close it safely without squeezing contaminated materials to avoid aerosolization.
●Reprocess the nondisposable PPE.
Inside the catheterization laboratory:
●Wait until the patient is out of the room; close the door.
●Perform hand hygiene over the gloves.
●Peel off gown and gloves together and roll inside, slowly and carefully, avoiding aerosolization.
●If gloves are removed separately, touch only the external part (use glove-in-glove or beak technique).
●Perform hand hygiene (over the internal gloves).
●Remove face shield and/or goggles, avoiding contact with face and eyes, and dispose them safely or put into a separate container for reprocessing.
●Perform hand hygiene (over the internal gloves).
●Remove hair cover and dispose it safely.
●Remove shoe covers and dispose them safely.
●Perform hand hygiene (over the internal gloves).
●Remove internal gloves and dispose them safely.
●Perform hand hygiene.
●Step out of the catheterization laboratory and immediately close the door.
Outside the operating room:
●Put on another pair of gloves
●Remove facial respirator without touching the front side of the respirator
●Remove the gloves
●Remove lead apron
●Perform hand hygiene with soap, water, and alcohol gel/rub
No guidelines have been issued that address whether health care workers exposed to blood of COVID-19 patients should be managed any differently than usual.
Cardiopulmonary resuscitation — A discussion of cardiopulmonary resuscitation in COVID-19 patients is presented separately. (See "Advanced cardiac life support (ACLS) in adults", section on 'Resuscitation of patients with COVID-19'.)
Prognosis — Prognosis for patients with COVID-19 is worse with comorbidities such as cardiovascular disease. In an early report from China, mortality was 10.5 percent in patients with cardiovascular disease [38].
Mortality rates appear to increase significantly with increasing age; case fatality rates <1 percent have been reported for those under 50 years of age, with rates approaching 15 percent for patients 80 years of age or older [21]. Similarly, mortality increases with disease severity, as there were no deaths reported among the mild or severe cases in the Chinese cohort, but mortality approached 50 percent among critically-ill patients [21].
Underlying medical comorbidities appear to significantly impact COVID-19 severity and mortality. Patients with underlying cardiovascular disease and hypertension have been reported to have significantly high case fatality rates compared with patients without these underlying comorbidities (10.5 and 6 percent mortality, respectively, compared with 0.9 percent mortality without underlying comorbidities) [21,39].
In addition, reports have found that the higher the troponin level, the worse the prognosis. This has been generally found in other situations. (See "Troponin testing: Clinical use", section on 'Prognosis' and "Troponin testing: Clinical use", section on 'General population'.)
STABLE CORONARY ARTERY DISEASE PATIENTS — We do not change our usual management of CAD in patients with COVID-19 infection, with one exception: We attempt to delay elective revascularization procedures in patients for whom the indication is relief of symptoms. Such an approach protects the patient and health care workers from potential viral exposure. For patients who must have revascularization for reasons such as extremely poor quality of life or prolongation of life, as with significant left main CAD, we test the patient for COVID-19 infection.
Decisions regarding the type of revascularization (eg, coronary artery bypass graft surgery versus percutaneous coronary intervention [PCI]) in these patients may be altered during the pandemic, favoring PCI as a method to shorten the duration of exposure of the patient to the hospital environment. We encourage heart team discussion with inclusion of the patient regarding these issues. We do not routinely test the patient for COVID-19 infection in this setting.
None of the usual medications for the management of CAD, such as aspirin, beta blockers, statins, and nitrates, have been associated with worse outcomes in the setting of COVID-19 infection. We continue angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. This issue is discussed in detail elsewhere. (See "COVID-19: Management in hospitalized adults", section on 'ACE inhibitors/ARBs'.)
Patients admitted for management of COVID-19 — Many patients admitted for management of COVID-19 will have stable CAD. (See 'Epidemiology' above and "COVID-19: Management in hospitalized adults", section on 'General management issues'.)
Electrocardiogram — All patients in whom COVID-19 is suspected should have a baseline ECG performed at the time of entry into the hospital. Ideally, this would be a 12-lead ECG, but a single- or multi-lead ECG from telemetry monitoring may be adequate in this situation to minimize staff exposure to the patient. This will allow for documenting baseline QRS-T morphology should the patient develop signs/symptoms suggestive of myocarditis or an acute coronary syndrome (ACS). Additionally, the baseline ECG allows for documentation of the QT (and corrected QTc) interval. Importantly, QTc will need to be monitored if QT-prolonging therapies are initiated (eg, azithromycin, chloroquine, etc) to reduce the risk of acquired long QT syndrome. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management" and "COVID-19: Arrhythmias and conduction system disease", section on 'Patients receiving therapies that prolong the QT interval'.)
Troponin — Cardiac troponin elevation is seen in about 10 to 30 percent of hospitalized COVID-19 patients and is associated with a higher mortality [3,26,39]. Most patients with troponin elevation and COVID-19 do not have a clinical presentation suggestive of an ACS. (See 'Association between baseline CVD and COVID-19' above.)
The optimal use of troponin testing in hospitalized COVID-19 patients without suspected ACS is not known. Many centers obtain a troponin soon after admission in all patients, as it may have prognostic value and may serve as a useful baseline for comparison in patients who subsequently develop manifestations of possible myocardial injury (such as heart failure or arrhythmia) [40]. Other centers limit troponin testing in this setting to patients with a specific indication (such as suspected ACS based on clinical presentation or new onset heart failure), as the clinical value of troponin levels has not been established, and results may lead to unnecessary use of medical resources (eg, serial troponins, ECGs, and cardiology consultations for elevated troponin) [41]. (See "COVID-19: Evaluation and management of cardiac disease in adults".)
RECOMMENDATIONS OF OTHERS — Our approach to patients with COVID-19 and acute or chronic coronary artery disease is generally consistent with the position taken by major society organizations [42-44].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: COVID-19 – Index of guideline topics".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: COVID-19 overview (The Basics)")
●Basics topic (see "Patient education: COVID-19 vaccines (The Basics)")
SUMMARY AND RECOMMENDATIONS
●A relatively high percent of patients admitted with COVID-19 will have underlying coronary artery disease (CAD). For most, symptoms of CAD will not be present on admission. (See 'Epidemiology' above.)
●It is likely that COVID-19 directly and indirectly affects the cardiovascular system, causing or contributing to acute coronary syndrome (ACS), myocarditis, and electrical heart disease. (See 'Impact on the cardiovascular system' above.)
●Health care providers should make every effort to persuade patients to seek proper evaluation if the diagnosis of ACS is considered. (See 'Acute coronary syndrome patients' above.)
●In patients with known or suspected COVID-19, we approach the diagnosis and management of ST-elevation myocardial infarction (MI) similar to those without. On occasion, it is reasonable to liberalize the use of fibrinolytic therapy relative to primary percutaneous coronary intervention. (See 'ST-elevation myocardial infarction' above.)
●In patients with known or suspected COVID-19, we approach the diagnosis and management of non-ST-elevation MI similar to those without. (See 'Non-ST-elevation myocardial infarction' above.)
●We do not change our usual management of CAD in patients with COVID-19 infection with one exception: We attempt to delay elective revascularization procedures in patients for whom the indication is relief of symptoms. (See 'Stable coronary artery disease patients' above.)
●For hospitalized COVID-19 patients with stable CAD, some centers routinely obtain a baseline cardiac troponin while others do not. (See 'Troponin' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Duane Pinto, MD, MPH, who contributed to earlier versions of this topic review.
