{"product_id":"covid-19-and-heart-disease-how-the-sars-cov-2-virus-affects-your-cardiovascular-system","title":"COVID-19 and Heart Disease: How the SARS-CoV-2 Virus Affects Your Cardiovascular System","description":"\u003cp\u003eCOVID-19 is far more than a respiratory illness — it can deeply affect the heart, from triggering heart attacks and dangerous heart rhythms to causing heart failure and sudden death. This review, written by cardiologists at the University of Arizona, explains exactly how the SARS-CoV-2 virus damages the cardiovascular system, what heart complications doctors are seeing in hospitalized patients, and how treatments for COVID-19 can themselves pose cardiac risks. The article draws on early data from China, New York, and Europe — including findings from more than 72,000 patients — to help doctors and patients understand the cardiac side of this disease.\u003c\/p\u003e\n\n\u003ch1\u003eCOVID-19 and Heart Disease: How the SARS-CoV-2 Virus Affects Your Cardiovascular System\u003c\/h1\u003e\n\n\u003ch2\u003eTable of Contents\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\u003ca href=\"#ddn-key-points\"\u003eKey Points\u003c\/a\u003e\u003c\/li\u003e\n\n  \u003cli\u003e\u003ca href=\"#background\"\u003eBackground: Why This Research Matters\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#pathophysiology\"\u003eHow the Virus Invades the Body (Pathophysiology)\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#stages\"\u003eThree Clinical Stages of COVID-19 Infection\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#cardiac-manifestations\"\u003eHow COVID-19 Affects the Heart: Key Cardiovascular Complications\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#treatment-effects\"\u003eCardiac Effects of COVID-19 Treatments\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#management\"\u003eHow Doctors Manage Heart Patients With COVID-19\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#limitations\"\u003eLimitations of This Review\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#recommendations\"\u003eRecommendations for Patients\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#ddn-faq\"\u003eFrequently Asked Questions\u003c\/a\u003e\u003c\/li\u003e\n\u003cli\u003e\u003ca href=\"#source\"\u003eSource Information\u003c\/a\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003c!-- ddn:keypoints:start --\u003e\n\u003ch2 id=\"ddn-key-points\"\u003eKey Points\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003eCOVID-19 can damage the heart, causing arrhythmias, heart failure, and sudden death, not just lung problems.\u003c\/li\u003e\n\u003cli\u003eIn a 44,672-patient Chinese study, death rate was 10.5% with cardiovascular disease versus 2.3% overall.\u003c\/li\u003e\n\u003cli\u003eDo not stop ACE inhibitors or ARBs during COVID-19; evidence suggests they may be protective.\u003c\/li\u003e\n\u003cli\u003eHeart attacks in COVID-19 often involve inflammation or small clots, not blocked arteries; mortality was 72% in one 18-patient series.\u003c\/li\u003e\n\u003cli\u003eQT-prolonging COVID-19 treatments require daily ECG and electrolyte monitoring to prevent dangerous rhythms.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003c!-- ddn:keypoints:end --\u003e\n\n\n\u003ch2 id=\"background\"\u003eBackground: Why This Research Matters\u003c\/h2\u003e\n\n\u003cp\u003e\u003cstrong\u003eCoronavirus disease 2019 (COVID-19)\u003c\/strong\u003e is a serious illness caused by \u003cstrong\u003esevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)\u003c\/strong\u003e. The disease first emerged in Wuhan province, China, in late 2019. The virus is genetically related to the coronavirus responsible for the 2002 SARS outbreak, but it has spread far more widely.\u003c\/p\u003e\n\n\u003cp\u003eOn 11 March 2020, the World Health Organization (WHO) officially declared COVID-19 a global pandemic. Since that time, confirmed cases and deaths have risen daily — and it quickly became clear that this was not just a lung infection.\u003c\/p\u003e\n\n\u003cp\u003eThe symptoms of COVID-19 range from none at all (asymptomatic infection) to mild respiratory complaints and, in the worst cases, life-threatening heart and lung complications. Cardiac problems seen in COVID-19 patients include:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eAcute myocardial injury (damage to heart muscle cells)\u003c\/li\u003e\n  \u003cli\u003eArrhythmias (abnormal heart rhythms)\u003c\/li\u003e\n  \u003cli\u003eCardiogenic shock (when the heart cannot pump enough blood to the body)\u003c\/li\u003e\n  \u003cli\u003eSudden cardiac death\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eIn a large analysis of \u003cstrong\u003e72,314 patients\u003c\/strong\u003e with COVID-19 in China, researchers classified the illness severity as mild in \u003cstrong\u003e81.4%\u003c\/strong\u003e of cases, severe in \u003cstrong\u003e13.9%\u003c\/strong\u003e, and critical in \u003cstrong\u003e4.7%\u003c\/strong\u003e. While respiratory failure is the primary cause of death, the authors emphasize that cardiac complications also contribute significantly to overall death rates — and in some patients, they are the main cause of death.\u003c\/p\u003e\n\n\u003cp\u003eA study from New York found that the most common presenting symptoms of COVID-19 were cough (\u003cstrong\u003e79.4%\u003c\/strong\u003e), fever (\u003cstrong\u003e77.1%\u003c\/strong\u003e), shortness of breath (\u003cstrong\u003e56.5%\u003c\/strong\u003e), muscle aches (\u003cstrong\u003e23.8%\u003c\/strong\u003e), diarrhoea (\u003cstrong\u003e23.7%\u003c\/strong\u003e), and nausea and vomiting (\u003cstrong\u003e19.1%\u003c\/strong\u003e). Notably, many patients with heart involvement did not necessarily complain of chest pain first.\u003c\/p\u003e\n\n\u003ch3\u003eUnderlying Heart Conditions Are Common and Dangerous\u003c\/h3\u003e\n\n\u003cp\u003ePre-existing cardiovascular conditions are present in \u003cstrong\u003e8–25%\u003c\/strong\u003e of the overall COVID-19-infected population — and in a substantially higher proportion of those who die from the infection. A meta-analysis of eight studies from China involving \u003cstrong\u003e46,248 patients\u003c\/strong\u003e found that the most common pre-existing conditions among COVID-19 patients were:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eHypertension (high blood pressure): approximately \u003cstrong\u003e17.7%\u003c\/strong\u003e of patients\u003c\/li\u003e\n  \u003cli\u003eDiabetes mellitus: approximately \u003cstrong\u003e8.7%\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eCardiovascular disease: approximately \u003cstrong\u003e5.6%\u003c\/strong\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eAnother large analysis from the Chinese Center for Disease Control and Prevention, covering \u003cstrong\u003e44,672 confirmed cases\u003c\/strong\u003e, compared death rates according to pre-existing medical conditions. The case fatality rates were striking:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eCardiovascular disease: \u003cstrong\u003e10.5%\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eDiabetes: \u003cstrong\u003e7.3%\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eChronic respiratory disease: \u003cstrong\u003e6.3%\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eHypertension: \u003cstrong\u003e6.0%\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eCancer: \u003cstrong\u003e5.6%\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eOverall case fatality rate in the entire cohort: \u003cstrong\u003e2.3%\u003c\/strong\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eIn other words, a patient with pre-existing heart disease was more than four times more likely to die from COVID-19 than the average infected person. This pattern makes understanding the heart–virus connection a medical priority.\u003c\/p\u003e\n\n\u003ch2 id=\"pathophysiology\"\u003eHow the Virus Invades the Body (Pathophysiology)\u003c\/h2\u003e\n\n\u003cp\u003eTo understand how SARS-CoV-2 damages the heart, it helps to know how the virus enters cells. The virus contains four structural proteins: the \u003cstrong\u003espike (S) protein\u003c\/strong\u003e, \u003cstrong\u003eenvelope (E) protein\u003c\/strong\u003e, \u003cstrong\u003emembrane (M) protein\u003c\/strong\u003e, and \u003cstrong\u003enucleocapsid (N) protein\u003c\/strong\u003e. Of these, the spike protein is the key that unlocks human cells.\u003c\/p\u003e\n\n\u003cp\u003eThe S protein binds strongly to \u003cstrong\u003eangiotensin-converting enzyme 2 (ACE2) receptors\u003c\/strong\u003e — proteins found on the surface of cells in many organs, including the \u003cstrong\u003eheart, kidneys, intestine, lungs, brain, and liver\u003c\/strong\u003e. This explains why COVID-19 produces such a wide range of symptoms beyond the lungs, including atypical gastrointestinal complaints, cardiac and kidney injury, and neurological problems.\u003c\/p\u003e\n\n\u003cp\u003eOnce the virus enters cells through ACE2 receptors, it actually \u003cstrong\u003edown-regulates ACE2 expression\u003c\/strong\u003e — meaning the enzyme can no longer perform its usual organ-protective functions. This loss of protection may contribute to tissue injury in the heart and elsewhere.\u003c\/p\u003e\n\n\u003ch3\u003eWhat About Blood Pressure Medications?\u003c\/h3\u003e\n\n\u003cp\u003eA critical question early in the pandemic was whether \u003cstrong\u003eACE inhibitors (ACEI)\u003c\/strong\u003e and \u003cstrong\u003eangiotensin receptor blockers (ARB)\u003c\/strong\u003e — common blood pressure medications — increased the risk of COVID-19 infection. These drugs are known to increase the number of ACE2 receptors on the surface of heart, lung, and intestinal cells, which raised a theoretical concern that they might give the virus more doorways into cells.\u003c\/p\u003e\n\n\u003cp\u003eHowever, the evidence reviewed here suggests the opposite may be true. Experimental studies in mice showed that blocking the renin-angiotensin-aldosterone system (RAAS) reduced lung injury caused by the SARS-CoV-1 spike protein. Observational data in patients taking ACEI or ARB showed:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eA lower rate of severe COVID-19 disease\u003c\/li\u003e\n  \u003cli\u003eTrend toward lower levels of the inflammatory marker \u003cstrong\u003einterleukin-6 (IL-6)\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eIncreased CD3 and CD8 T-cell counts (immune cells) in the blood\u003c\/li\u003e\n  \u003cli\u003eA decreased peak viral load\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe authors note that ACEI\/ARB therapy may therefore be \u003cstrong\u003eprotective\u003c\/strong\u003e, particularly in low-level viraemia. At the time of writing, trials of \u003cstrong\u003elosartan\u003c\/strong\u003e (an ARB) in COVID-19 patients were ongoing. The authors advise patients not to stop these medications on their own.\u003c\/p\u003e\n\n\u003ch3\u003eThe Autopsy Evidence\u003c\/h3\u003e\n\n\u003cp\u003eExamining heart tissue from COVID-19 patients who died revealed important clues. In one autopsy study, researchers found:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eCardiomyocyte hypertrophy (enlarged heart muscle cells)\u003c\/li\u003e\n  \u003cli\u003eDegeneration and necrosis (cell death) of cardiomyocytes\u003c\/li\u003e\n  \u003cli\u003eMild interstitial hyperaemia and oedema (excess fluid)\u003c\/li\u003e\n  \u003cli\u003eInfiltration of lymphocytes, monocytes, and neutrophils (inflammatory immune cells)\u003c\/li\u003e\n  \u003cli\u003eNo virus particles found within the myocardial tissue itself\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eA second autopsy report showed scattered individual heart muscle cell death with lymphocytes located next to — but not surrounding — the dying cells, which may represent an early stage of viral myocarditis (inflammation of the heart muscle). The authors also explain that \u003cstrong\u003epericytes\u003c\/strong\u003e, cells that support tiny blood vessels, may become infected by the virus, leading to capillary endothelial dysfunction and individual cell death.\u003c\/p\u003e\n\n\u003ch2 id=\"stages\"\u003eThree Clinical Stages of COVID-19 Infection\u003c\/h2\u003e\n\n\u003cp\u003eResearchers described the immune response to COVID-19 as \u003cstrong\u003emultiphasic\u003c\/strong\u003e — developing in distinct stages that require different treatment approaches. This framework, originally proposed by Siddiqi and colleagues, helps doctors decide when to use supportive care versus more aggressive therapies:\u003c\/p\u003e\n\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003eStage 1 — Viral response \/ early infection:\u003c\/strong\u003e Constitutional symptoms (fever, fatigue), mild respiratory or gastrointestinal symptoms. Laboratory findings may show mild leukopenia (low white blood cell count) and lymphopenia (low lymphocyte count), elevated prothrombin time, D-dimer, LDH, CRP, ferritin, and IL-6. Procalcitonin may be normal. Treatment focuses on antimicrobial therapy and reducing immunosuppressants if needed.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eStage 2 — Inflammatory \/ pulmonary phase:\u003c\/strong\u003e Shortness of breath and hypoxia (low oxygen levels), with a PaO2\/FiO2 ratio below 300 and abnormal chest CT scans. Inflammatory markers and cardiac biomarkers (troponin, BNP) rise. Treatment shifts to supportive care, restrictive IV fluid strategy, antimicrobials, and immunotherapy as directed by infectious disease specialists.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eStage 3 — Hyperinflammatory \/ cytokine release storm:\u003c\/strong\u003e This is the most dangerous phase. Patients develop \u003cstrong\u003eARDS (acute respiratory distress syndrome)\u003c\/strong\u003e, sepsis, systemic inflammatory response syndrome (SIRS), cardiac failure, multi-organ dysfunction, shock, and \u003cstrong\u003edisseminated intravascular coagulation (DIC)\u003c\/strong\u003e — a condition in which blood clotting goes haywire. Inflammatory markers and cardiac biomarkers are markedly elevated. Patients require intensive care, often with ventilatory support and vasoactive medications.\u003c\/li\u003e\n\u003c\/ol\u003e\n\n\u003cp\u003eThe inflammatory cascade is closely linked to heart damage. Elevated levels of C-reactive protein (CRP), D-dimer, ferritin, IL-6, and lactate dehydrogenase (LDH) have been associated with higher mortality in COVID-19 patients, possibly due to a \u003cstrong\u003ecytokine storm\u003c\/strong\u003e — an overwhelming, uncontrolled immune response — or secondary haemophagocytic lymphohistiocytosis (an extreme inflammatory syndrome).\u003c\/p\u003e\n\n\u003ch2 id=\"cardiac-manifestations\"\u003eHow COVID-19 Affects the Heart: Key Cardiovascular Complications\u003c\/h2\u003e\n\n\u003ch3\u003eMyocardial Injury, Acute Coronary Syndrome, and Myocarditis\u003c\/h3\u003e\n\n\u003cp\u003e\u003cstrong\u003eMyocardial injury\u003c\/strong\u003e is defined as elevation of cardiac troponin (a protein released when heart muscle is damaged) above the 99th percentile of the upper reference limit. This finding has been observed in \u003cstrong\u003e7–17% of hospitalised COVID-19 patients\u003c\/strong\u003e. Importantly, the incidence rises dramatically with illness severity:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eAbout \u003cstrong\u003e22.2%\u003c\/strong\u003e of patients requiring intensive care showed myocardial injury\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e59%\u003c\/strong\u003e of patients who died had myocardial injury\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe mechanisms behind this injury are likely \u003cstrong\u003emultifactorial\u003c\/strong\u003e:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eAtherosclerotic plaque rupture (a cholesterol plaque breaking open)\u003c\/li\u003e\n  \u003cli\u003eCoronary vasospasm (sudden squeezing of heart arteries)\u003c\/li\u003e\n  \u003cli\u003eHypoxic injury to the vasculature (damage from low oxygen)\u003c\/li\u003e\n  \u003cli\u003eDirect endothelial injury (damage to blood vessel lining)\u003c\/li\u003e\n  \u003cli\u003eFormation of microthrombi (tiny blood clots in small vessels)\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe authors explain that myocardial injury and \u003cstrong\u003efulminant (sudden and severe) myocarditis\u003c\/strong\u003e can occur both from direct viral effects on heart muscle cells and from the body's exaggerated immune response to the virus.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eAcute coronary syndrome (ACS)\u003c\/strong\u003e can be one of the initial presentations of COVID-19, ranging from \u003cstrong\u003eST-elevation myocardial infarction (STEMI)\u003c\/strong\u003e — the most severe type of heart attack — to \u003cstrong\u003eTakotsubo cardiomyopathy\u003c\/strong\u003e (stress-induced \"broken heart syndrome\"). Myocardial ischaemia and infarction may result from plaque rupture triggered by the stress response to the virus, or from blood clots secondary to hypercoagulability. \u003cstrong\u003eType 2 myocardial infarction\u003c\/strong\u003e can also occur when there is a mismatch between oxygen supply and demand in the heart.\u003c\/p\u003e\n\n\u003cp\u003eA striking case series of \u003cstrong\u003e18 COVID-19 patients in New York\u003c\/strong\u003e who experienced STEMI — 10 at initial presentation and 8 during hospitalisation — showed:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eWide variability in how patients presented\u003c\/li\u003e\n  \u003cli\u003eA high prevalence of non-obstructive coronary disease (\u003cstrong\u003e33%\u003c\/strong\u003e of those who underwent cardiac catheterisation had no significant blockages)\u003c\/li\u003e\n  \u003cli\u003eA remarkably poor prognosis: \u003cstrong\u003e72% mortality\u003c\/strong\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThis suggests that many \"heart attacks\" in COVID-19 patients are not caused by blocked arteries but by inflammation, spasm, or small-vessel clotting. Acute \u003cstrong\u003evirus-negative lymphocytic myocarditis\u003c\/strong\u003e has also been associated with SARS-CoV-2 respiratory infection, and some reports showed improvement in cardiac biomarkers with lopinavir\/ritonavir and hydroxychloroquine treatment.\u003c\/p\u003e\n\n\u003cp\u003eThe authors caution that any rise in troponin should be interpreted in the clinical context, and that invasive angiography or coronary CT angiography may be needed to distinguish between a classic heart attack and myocarditis.\u003c\/p\u003e\n\n\u003ch3\u003eCardiac Arrhythmias (Heart Rhythm Problems)\u003c\/h3\u003e\n\n\u003cp\u003eElevated cytokine levels trigger systemic inflammation and myocardial injury — both of which can set the stage for \u003cstrong\u003eatrial and ventricular arrhythmias\u003c\/strong\u003e. New-onset, dangerous rapid rhythms, such as \u003cstrong\u003esustained monomorphic ventricular tachycardia (VT)\u003c\/strong\u003e and \u003cstrong\u003epolymorphic VT\u003c\/strong\u003e, in a patient with elevated cardiac biomarkers should raise suspicion for myocarditis.\u003c\/p\u003e\n\n\u003cp\u003eSpecific data from the early studies included:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eAmong \u003cstrong\u003e137 patients\u003c\/strong\u003e admitted for COVID-19 in Hubei province, heart palpitations were a presenting symptom in \u003cstrong\u003e7.3%\u003c\/strong\u003e of patients.\u003c\/li\u003e\n  \u003cli\u003eIn a study of \u003cstrong\u003e138 hospitalised COVID-19 patients\u003c\/strong\u003e, arrhythmia occurred in \u003cstrong\u003e16.7%\u003c\/strong\u003e — and was far more common in intensive care unit (ICU) patients than in non-ICU patients (\u003cstrong\u003e44.4% vs 6.9%, p \u0026lt; 0.001\u003c\/strong\u003e).\u003c\/li\u003e\n  \u003cli\u003eComplete heart block and atrial fibrillation have both been reported in COVID-19 patients.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe authors stress that these rhythm disturbances can be deadly, particularly when combined with the effects of COVID-19 therapies that prolong the heart's electrical recovery time (QT interval).\u003c\/p\u003e\n\n\u003ch3\u003eHeart Failure and Cardiogenic Shock\u003c\/h3\u003e\n\n\u003cp\u003eIncreased inflammatory cytokines and respiratory distress can make pre-existing left ventricular (LV) dysfunction worse — or trigger a new-onset cardiomyopathy (weakening of the heart muscle). New LV dysfunction may represent myocarditis, stress cardiomyopathy, or myocardial ischaemia, all of which increase the risk of death.\u003c\/p\u003e\n\n\u003cp\u003eIn the study by Zhou and colleagues, the incidence of heart failure was significantly higher in patients who did not survive COVID-19 compared with survivors:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eNon-survivors: \u003cstrong\u003e52%\u003c\/strong\u003e developed heart failure\u003c\/li\u003e\n  \u003cli\u003eSurvivors: \u003cstrong\u003e12%\u003c\/strong\u003e developed heart failure\u003c\/li\u003e\n  \u003cli\u003eDifference statistically significant at \u003cstrong\u003ep \u0026lt; 0.0001\u003c\/strong\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eRight heart failure is also common in this setting, driven by elevated pulmonary artery pressure from lung complications. In early stages, worsening of heart failure with preserved ejection fraction (a form of heart failure where the pumping function looks normal but the heart is stiff) can occur due to aggressive IV fluid resuscitation. In later stages, as cytokine levels surge, acute systolic heart failure leading to \u003cstrong\u003ecardiogenic shock\u003c\/strong\u003e has been reported.\u003c\/p\u003e\n\n\u003ch3\u003eThe Threat of Blood Clots\u003c\/h3\u003e\n\n\u003cp\u003eCOVID-19 strongly activates the coagulation (clotting) cascade. This leads to low platelet counts (thrombocytopaenia) and, in severe cases, dangerous hypercoagulability. Doctors have observed \u003cstrong\u003eischaemia of the fingers and toes\u003c\/strong\u003e — sometimes called \"COVID toes\" — as a result of small blood clots. There is a higher incidence of \u003cstrong\u003evenous and arterial thromboembolism\u003c\/strong\u003e (blood clots in veins and arteries) despite patients receiving preventive anticoagulation. Contributing factors include excessive inflammation, hypoxia (low oxygen), immobilisation, and diffuse intravascular coagulation.\u003c\/p\u003e\n\n\u003cp\u003eSome physicians have even used \u003cstrong\u003etissue plasminogen activator (tPA)\u003c\/strong\u003e, a clot-busting drug, with some improvement in ARDS patients. This highlights how central blood clotting is to severe COVID-19 disease — and to its heart complications.\u003c\/p\u003e\n\n\u003ch2 id=\"treatment-effects\"\u003eCardiac Effects of COVID-19 Treatments\u003c\/h2\u003e\n\n\u003cp\u003eThe medications used to treat COVID-19 can themselves put the heart at risk. The article notes that various \u003cstrong\u003eantivirals, antimalarials, immunomodulating medications, glucocorticoids, and convalescent plasma\u003c\/strong\u003e from recovered patients have been used with variable results. The Infectious Disease Society of America (IDSA) published treatment guidelines that doctors were asked to follow.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eChloroquine and hydroxychloroquine\u003c\/strong\u003e — initially promoted as possible treatments — work by making the inside of cellular compartments (phagolysosomes) more alkaline, which prevents the virus from properly attaching to ACE2 receptors. However, both drugs can \u003cstrong\u003eprolong the QTc interval\u003c\/strong\u003e, a measure of the heart's electrical recovery after each beat. A dangerously prolonged QTc increases the risk of a life-threatening rhythm called \u003cstrong\u003eTorsades de Pointes\u003c\/strong\u003e.\u003c\/p\u003e\n\n\u003cp\u003eResearchers highlighted two important clinical studies with sobering results:\u003c\/p\u003e\n\n\u003cp\u003eFirst, a \u003cstrong\u003eFrench study of 181 hospitalised COVID-19 patients\u003c\/strong\u003e with oxygen requirements found \u003cstrong\u003eno evidence of clinical efficacy\u003c\/strong\u003e for hydroxychloroquine — despite earlier small studies suggesting it reduced viral carriage.\u003c\/p\u003e\n\n\u003cp\u003eSecond, a randomised trial of \u003cstrong\u003eremdesivir\u003c\/strong\u003e in adult patients with severe COVID-19 admitted to Chinese hospitals found that the drug was \u003cstrong\u003enot associated with a statistically significant difference\u003c\/strong\u003e in time to clinical improvement compared with placebo. (The original article text is cut off mid-sentence at this point, but this finding — later revised by additional trials — was the state of knowledge at the time of publication.)\u003c\/p\u003e\n\n\u003cp\u003eBecause COVID-19 therapies frequently interact with heart medications, doctors must check for drug–drug interactions, especially with antiplatelet agents, anticoagulants, and antiarrhythmic drugs.\u003c\/p\u003e\n\n\u003ch2 id=\"management\"\u003eHow Doctors Manage Heart Patients With COVID-19\u003c\/h2\u003e\n\n\u003cp\u003eThe review proposes a simplified management algorithm for cardiovascular disease in COVID-19 patients. Here are the key points translated for patients:\u003c\/p\u003e\n\n\u003ch3\u003eFor Heart Attacks (ACS, STEMI, NSTEMI)\u003c\/h3\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eNSTEMI (non-ST-elevation heart attack):\u003c\/strong\u003e Doctors check an ECG and troponin if acute coronary syndrome is suspected. Standard medications include aspirin, heparin (a blood thinner), statins (cholesterol-lowering drugs), and beta-blockers (if no slow heart rate or shock). Drug interactions are assessed. Cardiac catheterisation is performed if there is high suspicion of acute coronary blockage; otherwise, a coronary CT angiogram may be used in stable patients.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSTEMI (ST-elevation heart attack):\u003c\/strong\u003e Considered a medical emergency. Primary angioplasty (PCI) is the preferred treatment. Thrombolytic (clot-busting) therapy is controversial but may be used for lower-risk STEMI if an interventional cardiologist is not available. A bedside echocardiogram is recommended if there is any clinical uncertainty.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eIf no angiographic disease is found:\u003c\/strong\u003e Patients are monitored and treated for myocarditis complications, including heart failure, arrhythmia, thromboembolism, and risk factor modification.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch3\u003eFor Myocarditis and Myocardial Injury\u003c\/h3\u003e\n\n\u003cul\u003e\n  \u003cli\u003eEchocardiogram to assess left ventricular function\u003c\/li\u003e\n  \u003cli\u003eTroponin trend to distinguish from Type 1 heart attack and to assess prognosis (along with BNP)\u003c\/li\u003e\n  \u003cli\u003eArrhythmia monitoring, with electrophysiology (EP) consultation if dangerous rhythms appear\u003c\/li\u003e\n  \u003cli\u003eInotropes and vasopressors for haemodynamic instability with LV dysfunction\u003c\/li\u003e\n  \u003cli\u003eGuideline-directed medical therapy for cardiomyopathy\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eExercise restriction for 3–6 months\u003c\/strong\u003e to prevent sudden cardiac death in patients recovering from myocarditis\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch3\u003eFor Heart Failure and Shock\u003c\/h3\u003e\n\n\u003cul\u003e\n  \u003cli\u003eBNP, troponin, and echocardiogram to assess new-onset heart failure\u003c\/li\u003e\n  \u003cli\u003eTelemetry (continuous heart monitoring) for arrhythmia detection\u003c\/li\u003e\n  \u003cli\u003eStandard heart failure management: daily weight, input\/output tracking, diuretics (water pills), and close monitoring of electrolytes and kidney function\u003c\/li\u003e\n  \u003cli\u003eRestricted fluids and blood products due to high risk of cardiopulmonary decompensation; concentrated IV drips are preferred\u003c\/li\u003e\n  \u003cli\u003eAvoid nonsteroidal anti-inflammatory drugs (NSAIDs)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eContinue ACE inhibitors, ARBs, or ARNI\u003c\/strong\u003e (heart failure medications) in otherwise stable patients who are at risk for, being evaluated for, or infected with COVID-19 — unless they become hypotensive (low blood pressure) or develop kidney failure\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch3\u003eFor Shock\u003c\/h3\u003e\n\n\u003cul\u003e\n  \u003cli\u003eShock is defined as systolic blood pressure below \u003cstrong\u003e90 mmHg for more than 15 minutes\u003c\/strong\u003e with impaired organ perfusion, or urine output below \u003cstrong\u003e30 mL per hour\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eDoctors check mixed venous oxygen saturation to distinguish different types of shock\u003c\/li\u003e\n  \u003cli\u003eConservative fluid resuscitation with crystalloids preferred over colloids\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eNorepinephrine\u003c\/strong\u003e is the first-line drug to stabilise blood pressure; transition to inotropes when clinically indicated\u003c\/li\u003e\n  \u003cli\u003eInhaled pulmonary vasodilators (such as inhaled nitric oxide) should be given through a closed system to prevent aerosolisation of the virus\u003c\/li\u003e\n  \u003cli\u003eECMO (extracorporeal membrane oxygenation) and mechanical circulatory support devices are reserved for highly selected cases\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch3\u003eFor Arrhythmias and QTc Prolongation\u003c\/h3\u003e\n\n\u003cp\u003eMany COVID-19 therapies prolong the QTc interval, so monitoring is essential. The authors provide specific thresholds and actions:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eTelemetry monitoring and at least \u003cstrong\u003edaily QTc assessment\u003c\/strong\u003e for patients on high-risk therapy\u003c\/li\u003e\n  \u003cli\u003eKeep blood potassium above \u003cstrong\u003e4.5 mEq\/L\u003c\/strong\u003e and magnesium above \u003cstrong\u003e2.2 mg\/dL\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eIf QTc is \u003cstrong\u003e≥470 ms in men\u003c\/strong\u003e or \u003cstrong\u003e≥480 ms in women\u003c\/strong\u003e but below 500 ms: close surveillance and stop QT-prolonging medications\u003c\/li\u003e\n  \u003cli\u003eIf QTc is \u003cstrong\u003e\u0026gt;500 ms\u003c\/strong\u003e (or \u003cstrong\u003e\u0026gt;550 ms\u003c\/strong\u003e in the presence of bundle branch block), or if QTc increases by more than \u003cstrong\u003e60 ms\u003c\/strong\u003e after starting a drug: apply pacer pads, stop the QT-prolonging medication, and maintain heart rate above 80 beats per minute with isoproterenol or dobutamine\u003c\/li\u003e\n  \u003cli\u003eFor \u003cstrong\u003eTorsades de Pointes (TdP):\u003c\/strong\u003e IV magnesium \u003cstrong\u003e2–4 grams\u003c\/strong\u003e, maintain heart rate above 80 bpm (with beta-agonists or temporary pacing)\u003c\/li\u003e\n  \u003cli\u003eFor ventricular tachycardia (VT): \u003cstrong\u003eamiodarone 150 mg IV bolus\u003c\/strong\u003e followed by infusion of 1 mg\/min if QTc is below 450 ms; or \u003cstrong\u003elidocaine\u003c\/strong\u003e (bolus 75–100 mg, then infusion 0.5–2 mg\/min) if QTc is above 550 ms\u003c\/li\u003e\n  \u003cli\u003eFor supraventricular tachycardia (SVT) including atrial fibrillation: \u003cstrong\u003eadenosine 6–12 mg IV push\u003c\/strong\u003e for acute management; beta-blockers may be preferred over calcium channel blockers depending on LV function\u003c\/li\u003e\n  \u003cli\u003eLenient rate control is favoured — \"permissive tachycardia\" is acceptable in this setting\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch3\u003eCardiac Arrest in COVID-19 Patients\u003c\/h3\u003e\n\n\u003cp\u003eThe authors emphasise addressing goals of care early and periodically with all patients. For cardiac arrest, standard advanced cardiac life support (ACLS) protocols should be followed, but with important pandemic-specific modifications:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eUse a mechanical CPR device if available\u003c\/li\u003e\n  \u003cli\u003eWear full personal protective equipment (PPE) per hospital protocol before starting resuscitation\u003c\/li\u003e\n  \u003cli\u003eMinimise code team size to limit exposure of health care workers\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch3\u003eSpecial Considerations for Transplant Patients\u003c\/h3\u003e\n\n\u003cp\u003eFor heart transplant patients on immunosuppressive medications, doctors should discuss reducing immunosuppression — especially antimetabolites — due to the risk of severe infection. Patients on chronic steroids may need stress-dose steroids to prevent adrenal insufficiency.\u003c\/p\u003e\n\n\u003ch2 id=\"limitations\"\u003eLimitations of This Review\u003c\/h2\u003e\n\n\u003cp\u003eThis article was written in the early phase of the pandemic (received for review April–May 2020, published online 5 June 2020), and the authors note that many treatment recommendations were based on limited data. Several important caveats apply:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003eMuch of the evidence came from observational studies and small case series, not large randomised controlled trials\u003c\/li\u003e\n  \u003cli\u003eThe benefits of hydroxychloroquine and remdesivir were still uncertain — later trials would go on to clarify (and often overturn) early impressions\u003c\/li\u003e\n  \u003cli\u003eThe long-term cardiac effects of COVID-19 in survivors were not yet known at the time of publication\u003c\/li\u003e\n  \u003cli\u003eThe interaction between ACE inhibitors\/ARBs and COVID-19 risk was still being studied, with definitive trials pending\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eDespite these limitations, the core message has held up well: COVID-19 is a cardiovascular disease as much as a respiratory one, and pre-existing heart disease significantly worsens outcomes.\u003c\/p\u003e\n\n\u003ch2 id=\"recommendations\"\u003eRecommendations for Patients\u003c\/h2\u003e\n\n\u003cp\u003eBased on this review, here is practical advice for patients concerned about COVID-19 and heart disease:\u003c\/p\u003e\n\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003eDo not stop your heart medications.\u003c\/strong\u003e If you take ACE inhibitors or ARBs for blood pressure or heart failure, continue them unless your doctor specifically tells you otherwise. Stopping them can cause rebound hypertension and increase cardiac risk.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eKnow the warning signs.\u003c\/strong\u003e Chest pain, palpitations, severe shortness of breath, fainting, or rapid heartbeats during a COVID-19 illness warrant urgent medical evaluation. Remember that in one series, heart attack was the first sign of COVID-19 in some patients.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eControlled heart disease makes a difference.\u003c\/strong\u003e The patients at highest risk are those with uncontrolled hypertension, diabetes, and established cardiovascular disease. Optimising these conditions — under medical supervision — may reduce your risk.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eRecognise that COVID-19 treatment involves heart monitoring.\u003c\/strong\u003e If you are hospitalised and receive medications that prolong the QTc interval, expect daily ECGs and blood tests. This monitoring is designed to protect you from dangerous rhythm problems.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eRecovery takes time.\u003c\/strong\u003e If you are diagnosed with myocarditis from COVID-19, plan for exercise restriction for 3–6 months to reduce the risk of sudden cardiac death — even if you feel better.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003ePrevention remains the most vital step.\u003c\/strong\u003e The authors remind readers that preventing the spread of infection through quarantine and personal hygiene is the single most important strategy, and this is especially true for patients with underlying heart disease.\u003c\/li\u003e\n\u003c\/ol\u003e\n\n\u003c!-- ddn:faq:start --\u003e\n\u003ch2 id=\"ddn-faq\"\u003eFrequently Asked Questions\u003c\/h2\u003e\n\u003ch3\u003eCan COVID-19 really affect the heart even if you don't have chest pain?\u003c\/h3\u003e\n\u003cp\u003eYes. COVID-19 can cause heart muscle damage, abnormal heart rhythms, heart failure, and sudden death. In a New York study, the most common symptoms were cough, fever, and shortness of breath, not chest pain. Some patients had a heart attack as their first sign of COVID-19.\u003c\/p\u003e\n\u003ch3\u003eHow much higher is the risk of dying from COVID-19 if you already have heart disease?\u003c\/h3\u003e\n\u003cp\u003eIn a Chinese analysis of 44,672 confirmed cases, the death rate was 10.5% for people with cardiovascular disease, compared with 2.3% overall. That means someone with pre-existing heart disease was more than four times more likely to die from COVID-19 than the average infected person.\u003c\/p\u003e\n\u003ch3\u003eShould I stop taking my blood pressure medicine (ACE inhibitor or ARB) during the COVID-19 pandemic?\u003c\/h3\u003e\n\u003cp\u003eNo. The article says patients should not stop these medications on their own. Evidence reviewed suggests ACE inhibitors and ARBs may actually be protective against severe COVID-19, possibly by reducing lung injury. Stopping them can cause rebound high blood pressure and increase cardiac risk.\u003c\/p\u003e\n\u003ch3\u003eWhat heart complications can happen in hospitalized COVID-19 patients?\u003c\/h3\u003e\n\u003cp\u003eComplications include myocardial injury (damage to heart muscle cells), arrhythmias, heart failure, cardiogenic shock, and blood clots. Myocardial injury was seen in 7–17% of hospitalized patients, but in 22.2% of ICU patients and 59% of patients who died. Dangerous rhythms were more common in ICU patients.\u003c\/p\u003e\n\u003ch3\u003eWhy do COVID-19 patients get heart attacks even without blocked arteries?\u003c\/h3\u003e\n\u003cp\u003eIn a New York series of 18 COVID-19 patients with ST-elevation heart attacks, 33% of those who had cardiac catheterization showed no significant blockages. The authors say inflammation, coronary spasm, or tiny blood clots in small vessels can cause heart muscle damage, not just plaque rupture. These patients had a 72% mortality rate.\u003c\/p\u003e\n\u003ch3\u003eCan the medications used to treat COVID-19 cause heart rhythm problems?\u003c\/h3\u003e\n\u003cp\u003eYes. Drugs like chloroquine and hydroxychloroquine can prolong the QTc interval, which increases the risk of a dangerous rhythm called Torsades de Pointes. Therefore, hospitalized patients receiving these therapies should have daily ECGs and blood tests to monitor potassium, magnesium, and QTc.\u003c\/p\u003e\n\u003c!-- ddn:faq:end --\u003e\n\n\u003ch2 id=\"source\"\u003eSource Information\u003c\/h2\u003e\n\n\u003cp\u003eThis patient-friendly article is based on a peer-reviewed scientific review:\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eOriginal title:\u003c\/strong\u003e \"SARS-CoV-2 Infection and Cardiovascular Disease: COVID-19 Heart\"\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eAuthors:\u003c\/strong\u003e Bishnu P. Dhakal, MD; Nancy K. Sweitzer, MD, PhD; Julia H. Indik, MD, PhD; Deepak Acharya, MD, MSPH; Preethi William, MD — Sarver Heart Center, University of Arizona, Tucson, AZ, USA.\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003ePublication:\u003c\/strong\u003e \u003cem\u003eHeart, Lung and Circulation\u003c\/em\u003e (2020), Volume 29, pages 973–987. Published by Elsevier on behalf of the Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ).\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eDOI:\u003c\/strong\u003e https:\/\/doi.org\/10.1016\/j.hlc.2020.05.101\u003c\/p\u003e\n\n\u003cp\u003e\u003cstrong\u003eNote:\u003c\/strong\u003e This patient-friendly article is based on peer-reviewed research and is intended for educational purposes. It does not replace individual medical advice. Patients should always consult their own healthcare provider regarding their specific medical situation.\u003c\/p\u003e","brand":"DiagnosticDetectives.Com","offers":[{"title":"Default Title","offer_id":47423016894620,"sku":null,"price":0.0,"currency_code":"EUR","in_stock":true}],"url":"https:\/\/diagnosticdetectives.es\/products\/covid-19-and-heart-disease-how-the-sars-cov-2-virus-affects-your-cardiovascular-system","provider":"DiagnosticDetectives.Com","version":"1.0","type":"link"}