February 2021 Issue
Heart Health & COVID-19
By Karen Collins, MS, RDN, CDN, FAND
Vol. 23, No. 2, P. 18
Today’s Dietitian examines how the virus impacts the cardiovascular system and offers nutrition strategies for optimal patient care.
It’s been more than a year since COVID-19 reached the United States. And while it primarily affects the respiratory system, the fact is it’s a multisystem disease that also impacts cardiovascular health. Many questions remain amid ongoing research about the short- and long-term implications for heart health.
This article provides the background dietitians need to effectively participate as vital members of a multidisciplinary health care team and address questions patients and their families may ask based on the myriad headlines they read.
Impact on Heart Health
COVID-19 is caused by the novel coronavirus known as severe acute respiratory syndrome (SARS)-CoV-2. Primary effects of COVID-19 involve the lungs, where it causes severe inflammation that damages alveoli. Acute respiratory distress syndrome (ARDS) is the principal severe health effect and predominant cause of death from COVID-19. People who develop ARDS generally need ICU admission and mechanical ventilator support to breathe.1
However, COVID-19 and its treatment also can cause the following cardiac complications:
• Myocardial injury can occur from infiltration of SARS-CoV-2 into cardiac myocytes (heart muscle cells) or from inflammation or hypoxia (inadequate level of oxygen reaching the heart). This injury to the heart muscle can lead to cardiac dysfunction and arrhythmias, and is strongly linked with deaths from COVID-19.1-4
• Vascular inflammation begins in pulmonary capillaries in response to infiltration of SARS-CoV-2 into endothelial cells. These cells respond by releasing inflammatory cytokines and vascular adhesion molecules that aggravate inflammation within the lungs, and can circulate throughout the body creating systemic inflammation, which is a hallmark of severe COVID-19.1,5
• Thrombotic complications include venous thrombosis, pulmonary embolism, vasculitis, cardiomyopathy, and stroke. Thrombosis related to COVID-19 can stem from inflammation and dysfunction in the endothelium of pulmonary capillaries, platelet hyperactivation, and plaque rupture triggered by the infection.3,5,6
Other complications are possible as side effects of COVID-19 treatment.3 And research is underway to understand lingering effects that remain even after resolution of SARS-CoV-2 infection that can have multiple effects on cardiovascular health.7,8
COVID-Related Cardiovascular Risk
Early in 2020, the American Heart Association (AHA) established the AHA COVID-19 Cardiovascular Disease Registry to collect data from sites across the country.9 The registry included more than 22,500 patients by November 2020, and data through September 30, 2020, were shared at the 2020 AHA Scientific Sessions.
Research is ongoing to better understand the clinical course of COVID-19. Median incubation period from exposure to onset of symptoms is four to five days but may extend to 14 days. The acute mild phase of COVID-19 may last from five to 12 days with a variety of symptoms such as fever, cough, myalgia, and fatigue. Most people gradually recover from these symptoms, but during this time some develop dyspnea or other symptoms of ARDS and require hospitalization. Recovery may take six weeks or more. In about 20% of hospitalized patients in the AHA COVID-19 registry, the disease progressed, requiring mechanical ventilation and/or ICU admission.9,10
AHA registry data show in-hospital cardiovascular complications in 8.8% of people hospitalized with COVID-19. Of the COVID-19 deaths in the registry, 72% were due to ARDS and 10% due to cardiac causes. Although these cardiovascular complications occur in a relatively small percentage of people with COVID-19, James de Lemos, MD, cochair of the AHA COVID-19 CVD Registry Steering Committee, emphasizes that, given the scale of this pandemic, the cumulative number of these cardiovascular events is still large.9
Impact of Preexisting CVD Risk Factors
The association of COVID-19 and heart health is bidirectional; not only does COVID-19 cause cardiac complications, but preexisting CVD risk factors seem to increase risk of more severe forms of COVID-19.
In the AHA registry of COVID-19 hospital admissions, preexisting CVD or CVD risk factors were common. Among this group, 58% had hypertension, 45% had obesity (BMI greater than 30), 35% had diabetes, and 34% had hyperlipidemia.9
Obesity and Overweight
Obesity clearly increases risk of severe COVID-19. After adjusting for potential confounding variables, class I obesity (BMI 30 to 34.9) was associated with a 54% greater risk of requiring mechanical ventilation compared with people with a normal BMI. And this risk progressively increased to more than double the risk among people with class III obesity (BMI 40 and above).9
Obesity-related risk of mechanical ventilation or in-hospital death rises more sharply for younger adults, who may not consider themselves as being at high risk of severe COVID-19. Among people in the AHA registry hospitalized with COVID-19 who were aged 50 and younger, 85% either had obesity (58%) or overweight (27%). People aged 50 and younger with BMI of 40 or more were 36% more likely to die during hospitalization compared with people the same age with BMI of 25.11
Overweight doesn’t raise risk of severe COVID-19 as much as obesity, but it does have some influence. Compared with people with normal BMI, those in the AHA registry with BMI of 25 to 29.9 were 28% more likely to require mechanical ventilation.9
Preexisting CVD and Underlying CVD Risk Factors
COVID-19 seems to worsen preexisting CVD and underlying CVD risk factors. And these risk factors, in turn, increase risk of severe COVID-19, characterized by mechanical ventilation, ICU admission, cardiovascular complications, ARDS, or pneumonia. Pooled analyses show that compared with people with no comorbidities, odds of severe COVID-19 range from two to more than six times greater in people with diabetes, hypertension, CVD, chronic kidney disease, or COPD.12-15
Race, Ethnicity, and Age
Race and ethnicity are strongly associated with severity of COVID-19. In the AHA COVID-19 registry, Black and Hispanic patients accounted for more than one-half of hospitalizations, and hospitalization occurred among people at younger ages. Once in the hospital, mortality and risk of major cardiovascular events didn’t differ by race or ethnicity. In analyzing these data, researchers concluded that the greater burden of mortality and morbidity seen in these groups stems from disproportionate exposure to the SARS-CoV-2 virus in occupational and other settings and a greater prevalence of relevant comorbidities.16
Older age also is associated with severity of COVID-19. In part, this relates to age-related decline in immune function. But impaired immune function and excess inflammation also can stem from malnutrition or inactivity due to functional limitations. And preexisting comorbidities can cause endothelial dysfunction, a proinflammatory state, and alterations in the innate immune response.15,17,18
What’s Behind the Cardiovascular Risk?
Dietitians may be asking, “What is it about COVID-19 that can potentially exacerbate cardiovascular risk factors and preexisting CVD or lead to new cardiovascular injury and complications?” Biomarkers of acute cardiac injury and coagulation are associated with worse prognosis, according to preliminary findings from COVID-19 studies.19
People who develop ARDS in severe COVID-19 experience difficulty breathing and have low blood oxygen, which may lead directly to respiratory failure as a primary cause of death. As SARS-CoV-2 infects and destroys lung cells, it triggers a local immune response with release of cytokines, attracting macrophages, monocytes, and T cells that promote further inflammation. A healthy immune system usually can respond to the infection, eliminate infected cells before the virus spreads, and clear neutralized viruses and damaged cells.20
However, in some people, a dysfunctional immune response occurs, with further accumulation of immune cells in the lungs and overproduction of proinflammatory cytokines. This can cause severe lung damage and create a “cytokine storm” that produces uncontrolled inflammation resulting in multiorgan damage, leading to cardiac, hepatic, and renal system organ failure.20
Acute Myocardial Injury
Acute myocardial injury is indicated by ECG abnormalities and elevated levels of cardiac biomarkers. High-sensitivity cardiac troponin, or hs-cTn, a protein that regulates heart contraction, is a sensitive marker that begins rising within hours of heart damage. The mechanisms of how this myocardial injury occurs are still unclear, but it seems to be largely attributable to advanced systemic inflammation.17 In a small proportion of people with COVID-19, SARS-CoV-2 also may infect the myocardium directly, resulting in viral myocarditis. Biomarkers of myocardial injury are strongly associated with mortality from COVID-19.2
Arrhythmias and sudden cardiac arrest also are major cardiovascular complications of COVID-19. Myocardial injury and systemic factors such as fever, hypoxia, and electrolyte abnormalities all can trigger arrhythmias. Moreover, antiviral medications and antibiotics such as hydroxychloroquine and azithromycin used to treat COVID-19 can induce arrhythmias in some patients.17
Vascular inflammation resulting from the cytokine storm of COVID-19 is a major factor in many cardiovascular complications. The vascular endothelium is a single layer of cells that lines the inside of blood vessels and plays a vital role in regulating the balance between blood vessel constriction and dilation, vascular permeability, cell adhesion, and anticoagulation. A gel-like material, known as the glycocalyx, coats the endothelium and provides an antithrombotic surface. Researchers suggest the cytokine storm likely breaks down the glycocalyx coating, contributing to endothelial inflammation and dysfunction and a significant decrease in antithrombotic activity of the blood vessel lining and increased risk of thrombotic events. SARS-CoV-2 also can directly infect endothelial cells, leading to changes that promote vasoconstriction and thrombogenesis.3,5
Hypercoagulability and Increased Thromboembolic Events
Hypercoagulability is a state of increased clot formation that occurs in COVID-19 due to elevated circulating prothrombotic factors, increased fibrin formation, greater clot strength, and decreased clot degradation. Especially in the setting of blood vessel endothelium damage and patients’ immobilization in bed, it leads to increased thromboembolic events, particularly deep vein thrombosis and pulmonary embolism, as common complications among people with severe COVID-19. And although arterial thrombosis is uncommon in other infection-related coagulation disorders, in COVID-19, plaque rupture or clot formation in arteries can occur, leading to stroke, ischemic coronary disease, and acute coronary syndrome (decreased blood flow in the coronary arteries leaving the heart muscle unable to properly function, resulting in heart attack or angina that occurs suddenly, even at rest).3 Indicators of this coagulopathy are increased blood levels of D-dimer (a breakdown product of fibrin in blood clots, indicating occurrence of some coagulation) but relatively normal prothrombin time and only modestly reduced platelet counts.3,17
Long-Term Cardio Concerns
In addition to acute cardiovascular effects of COVID-19, long-term cardiovascular morbidity is a concern. Elevated cardiac troponin levels that indicate cardiac damage generally return to normal about a week after a heart attack. Yet a small prospective observational cohort study of people who recently recovered from COVID-19 identified cardiac damage two to three months after infection. Cardiovascular magnetic resonance imaging and high-sensitivity troponin levels revealed some cardiac damage or ongoing myocardial inflammation in 60% to 78% of patients, independent of preexisting conditions and severity of the acute illness. More research is needed to determine whether such findings are replicated, whether such damage eventually resolves, and whether it’s clinically consequential.7
With so much remaining to learn about COVID-19, development of strategies for nutrition care at various stages is ongoing.
For people hospitalized with severe COVID-19, the Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN) guidelines for nutrition therapy in COVID-19 requiring ICU care emphasize that when patients can’t maintain adequate oral intake, early enteral nutrition in critical care improves mortality and reduces infections.
COVID-19 imposes several unique adaptations to care. To reduce risk to health care providers and other patients, procedures should be adapted to minimize contamination of equipment and limit exposure to health care providers. For example, estimate energy requirements using weight-based equations rather than indirect calorimetry. The SCCM-ASPEN guidelines call for feeding to be initiated with low-dose enteral nutrition that’s hypocaloric, advancing slowly over the first week of critical illness to supply 70% to 80% of caloric requirements. Emphasis is on achieving high protein intake, with a goal of 1.2 to 2 g/kg actual body weight (ABW)/day.21
Studies before the COVID-19 pandemic showed that even short periods of bed rest or hospitalization result in rapid loss of muscle mass and physical function, even in younger adults after only a few days. Risk of sarcopenia is magnified by age-related anabolic resistance to effects of activity or protein consumption, and by inflammation-related upregulation of catabolic pathways and downregulation of anabolic pathways. Thus, the cytokine storm in patients with severe COVID-19 not only contributes directly to tissue damage but also may contribute to sarcopenia.18,22
When oral intake is possible, severe coughing and fear of aspiration can limit people’s ability to eat adequately, so attention to intake is important. Overall, meeting nutritional needs is complicated during COVID-19 by the characteristic loss of taste and smell and poor appetite, so enhancing food’s flavor may improve intake.23
Nutrition care remains a challenge even though the highly catabolic phase of severe inflammation subsides following acute care of COVID-19. “When patients arrive at inpatient rehab following COVID-19, typically they’ve had tremendous weight and muscle mass loss,” says Rya Clark, RDN, LD, CNSC, clinical nutrition manager at TIRR Memorial Hermann in Houston. “A 20% weight loss in the last six to eight weeks is not unusual.” Malnutrition may have existed before COVID-19, developed while ill before hospitalization, or developed during hospitalization.24
“In the inpatient rehabilitation setting following COVID-19, our first goal is to identify and resolve any malnutrition,” Clark says. “By the time people are in the rehab setting, the inflammatory cytokine cascade has usually subsided and the exercise they are getting has strong benefits to support rebuilding muscle mass, so we generally provide protein in the range of 1.2 to 1.5 g/kg ABW, or 1.5 to 2 g/ kg ABW if BMI is over 30.”
Meeting nutritional needs is complicated, since these patients may have dysphagia following mechanical ventilation. The transition from tube feedings to a regular diet is a time with high risk of not meeting nutritional needs. Appetite stimulants may be helpful for some patients with persistent poor intake and continued weight loss. However, they can have side effects of particular concern for people with COVID-19. For example, some appetite stimulants increase risk of thromboembolic events, arrhythmias, or hypotension, according to guidelines developed by a multidisciplinary team at TIRR Memorial Hermann.25
As people progress toward going home, Clark says focus pivots to eating habits that reduce CVD risk factors. “We are slated to begin integrating dietitians more in the life skills training work. By cotreating patients along with occupational therapists, we can incorporate teaching about heart-healthy choices into teaching about meal planning, grocery shopping, and cooking.”
Roles for Dietitians in Preventive Care
Screening for malnutrition should be a routine part of clinical care, especially for patients at greatest risk, including those with functional impairments or comorbidities.18 For people with any cardiometabolic disease, the American Association of Clinical Endocrinologists emphasizes staying home as much as possible and washing hands, as well as getting adequate sleep and limiting alcohol.26
Dietitians can field questions about specific nutrients to bolster immune defenses in COVID-19. Although there are theoretical reasons for supplementation, even nutrients needed for immune function can be ineffective or counterproductive at extremely high levels.27 Here’s what the research says about the following nutrients.
• Zinc serum levels have been low in about 20% to 30% of US older adults in limited studies. Some studies suggest that 30 to 45 mg/day for a few months in people at risk can improve cell-mediated immune function. However, prolonged supplementation may cause copper deficiency that leads to anemia, leucopenia, or damage to the nervous system.25,27,28 Results from studies evaluating zinc in COVID-19 management aren’t yet available. Oral zinc supplements likely are safe for people who choose to take them as long as amounts don’t exceed 40 mg/day in adults, but safety is unclear regarding higher doses.29,30
• Vitamin C is important for immune response, but current studies don’t provide evidence supporting use to prevent or enhance treatment of COVID-19.27,29 Results of IV use of vitamin C don’t necessarily apply to oral food or supplement intake.27
• Vitamin D increases expression of some immune system components, and low serum D3 levels have been linked to increased risk of upper respiratory infections. Vitamin D deficiency or insufficiency frequently was seen in some small studies of people with severe COVID-19.31,32 However, levels at disease onset or at eight-week follow-up weren’t related to persistent symptom burden, lung function impairment, ongoing inflammation, or other disease outcomes. Vitamin D deficiency seen in people with factors related to greater COVID-19 severity could be a noncausal association. Some guidelines recommend 1,000 to 2,000 IU/day for people with prolonged hospitalization, limited outdoor access, or serum 25-hydroxyvitamin D levels below 20 or 30 ng/mL. Megadoses don’t further benefit immunity.25,32
Dietitians can remind patients that studies in isolated cells or laboratory animals provide a foundation for learning but don’t directly translate to amounts or circumstances for human consumption. It’s also helpful to clarify messages about “boosting” the immune system. A healthy immune system is important to attack harmful bacteria and viruses, but an immune system on overdrive leads to autoimmune diseases and chronic inflammation.
For RDs who aren’t directly working with COVID-19 patients, Clark says, “For dietitians who work on control of blood sugar or blood pressure with people who haven’t had COVID-19, we know that better control is linked to lower risk and better survival rates. Emphasize to them that there’s no better time to optimize control.”
Research on COVID-19 and its cardiovascular implications is ongoing. Dietitians can keep abreast of the science through reliable sources such as those listed in the sidebar.
— Karen Collins, MS, RDN, CDN, FAND, is a nutrition consultant specializing in cancer prevention and cardiometabolic health.
Sources for Scientific Updates on COVID-19
Academy of Nutrition and Dietetics
• Coronavirus (COVID-19) Professional Resource Hub: eatrightpro.org/coronavirus-resources
Centers for Disease Control and Prevention
• COVID-19 Science Update: cdc.gov/library/covid19/scienceupdates.html
• Interim Clinical Guidance for Management of Patients With Confirmed COVID-19: cdc.gov/coronavirus/2019-ncov/hcp/clinical-guidance-management-patients.html
• Information for Health Care Professionals About COVID-19: cdc.gov/coronavirus/2019-nCoV/hcp/index.html
Infectious Disease Society
• COVID-19 and Influenza — The Latest: What You Need to Know Today: idsociety.org/covid-19-real-time-learning-network
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22. Kirwan R, McCullough D, Butler T, Perez de Heredia F, Davies IG, Stewart C. Sarcopenia during COVID-19 lockdown restrictions: long-term health effects of short-term muscle loss. Geroscience. 2020;42(6):1547-1578.
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