SARS-CoV-2 enters host cells through interaction of its spike protein with the ACE2 receptor.
These receptors are highly expressed in tissues throughout the body, including the following organ systems4,5:
- Respiratory
- Cardiovascular
- Renal
- Endocrine
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Unchecked viral replication can trigger systemic inflammation across the heart, lungs, brain, kidneys, and vascular system.
This can cause endothelial impairment, which can lead to4-6:
- Vascular injury
- Clotting disruption
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This systemic inflammation and damage start during the acute phase of infection and lay the groundwork for PCCs, including long COVID.
COVID-19 can increase the risk of:
- New-onset medical conditions
- Exacerbation of existing conditions
- Persistent symptoms
Severe COVID-19 can increase these risks further.4,5,7,8
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*Specific to fatigue, brain fog, shortness of breath, and gastrointestinal symptoms.9
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In a meta-analysis of more than 19.2 million people, COVID-19 was associated with an additional 70% risk of new-onset hypertension within 7 months of infection compared with patients without COVID-19 (HR: 1.7; P<0.0001)15*
New-onset heart failure
In a meta-analysis of more than 21.4 million people, patients who had COVID-19 were 90% more likely to develop new-onset heart failure compared with patients who did not have COVID-19 (HR: 1.9; P<0.0001)†
Risk of heart failure was associated with age (P=0.001) and prior history of hypertension (P=0.02)16
New-onset major adverse cardiac events (MACE)
Hospitalized patients with COVID-19 were 2.3x more likely to develop new-onset MACE compared with COVID-19–negative controls up to 3.5 years following infection17‡
Exacerbation of preexisting CVD
Patients hospitalized with COVID-19 who had preexisting CVD§ were 3.3x more likely to develop myocardial injury|| compared to patients hospitalized with COVID-19 who did not have preexisting CVD (P<0.001)18¶
†Zuin, et al. conducted a systematic review and meta-analysis that summarized data from 5 studies in a total of 21,463,173 patients.16
‡Lu, et al. defined MACE as all-cause mortality or incidence of arrhythmias, inflammatory heart disease, thrombosis, cerebrovascular disorders, ischemic heart disease, and other cardiac disorders (defined as cardiogenic shock, cardiac arrest, heart failure, and non-ischemic cardiomyopathy).17
§Defined as a composite of a history of coronary artery disease, heart failure or cardiomyopathy, atrial fibrillation or flutter, severe valvular disease, peripheral arterial disease, and stroke or transient ischemic attack.18
||In a multivariable model compared with patients hospitalized for COVID-19 without pre-existing disease; myocardial injury was defined as troponin greater than the upper limit of normal for each site-specific assay.18
¶Sritharan, et al. conducted an observational cohort study in Australia with a total study population of N=1567.18
New-onset diabetes
In a systematic review summarizing data for more than 4.3 million COVID-19 patients, ~1.4% developed new-onset diabetes, more than twice the estimated rate seen in the general US population in 202319,20*
Persistent diabetes
Persistent diabetes developed in 14.8% (P<0.001) of prediabetic patients hospitalized with COVID-19—3.5x the rate observed in prediabetic patients without severe COVID-19 (4.2%, P>0.05) at 5-month follow-up21
Severe COVID-19 was found to increase the risk of new-onset*
• Asthma 1.8x (P=0.019)
• COPD 2x (P<0.0001)
compared with patients without COVID-1922,23
Exacerbation of preexisting asthma
Patients with preexisting asthma and severe COVID-19 had a 5.1x risk of severe asthma exacerbation† and 7.3x risk of death‡ compared with patients without COVID-1924§
At 12 months post-infection, compared with propensity score-matched influenza patients, COVID-19 patients were more likely to develop25*
- ~3x acute kidney injury (P<0.0001)
- ~2x advanced chronic kidney disease (stage 3-5) (P<0.0001)
Significantly higher rates of new-onset dementia occurred in US veterans hospitalized with severe COVID-19 (3.0%) compared with matched hospitalized COVID-19–negative US veterans (1.9%) (P<0.001)26*
Exacerbation of preexisting neurological conditions
Severe COVID-19† was associated with neurologic worsening‡ in patients with multiple sclerosis and related disorders (P=0.001)27
†Conway, et al. defined moderate COVID-19 as “patients requiring hospitalization but not ICU-level care” and severe COVID-19 as “patients requiring ICU-level care.” In alignment with the CDC definition of severe outcomes of COVID-19 (hospitalization, admission to the ICU, intubation or mechanical ventilation, or death), both groups were collectively referred to as severe COVID-19 within this piece.27,28
‡Neurologic symptom worsening was defined as relapse, pseudorelapse, worsening of preexisting multiple sclerosis and related disease symptoms, development of other neurologic symptoms, or new gadolinium-enhancing or T2 lesions on brain MRI.27
Fatigue
At 6 months post-infection, fatigue was reported in 18% of hospitalized patients with COVID-19 and 26% of patients admitted to the ICU with COVID-19, 1.6x & 2.4x the rate observed in nonhospitalized patients with COVID-19 (11.1%)29
Shortness of breath
Hospitalized patients with COVID-19 had a 1.8x higher risk of being diagnosed with shortness of breath in the 6 months post-infection compared with nonhospitalized patients with COVID‑1930
Reduced walking ability
Beyond the acute phase, severe COVID-19 leaves a lasting impact, hindering31:
- Walking ability (P=0.001)
- Oxygen saturation during exercise (P=0.02)
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