• Vol. 50 No. 1, 52–60
  • 01 January 2021

Impact of cardiovascular diseases on severity of COVID-19 patients: A systematic review


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Introduction: Coronavirus disease 2019 (COVID-19) cases are increasing rapidly worldwide. Similar to Middle East respiratory syndrome where cardiovascular diseases were present in nearly 30% of cases, the increased presence of cardiovascular comorbidities remains true for COVID-19 as well. The mechanism of this association remains unclear at this time. Therefore, we reviewed the available literature and tried to find the probable association between cardiovascular disease with disease severity and mortality in COVID-19 patients. Methods: We searched Medline (via PubMed) and Cochrane Central Register of Controlled Trials for articles published until Sept 5, 2020. Nineteen articles were included involving 6,872 COVID-19 patients. Results: The random-effect meta-analysis showed that cardiovascular disease was significantly associated with severity and mortality for COVID-19: odds ratio (OR) 2.89, 95% confidence interval (CI) 1.98–4.21 for severity and OR 3.00, 95% CI 1.67–5.39 for mortality, respectively. Risk of COVID-19 severity was higher in patients having diabetes, hypertension, chronic obstructive pulmonary disease, malignancy, cerebrovascular disease and chronic kidney disease. Similarly, patients with diabetes, hypertension, chronic liver disease, cerebrovascular disease and chronic kidney disease were at higher risk of mortality. Conclusion: Our findings showed that cardiovascular disease has a negative effect on health status of COVID-19 patients. However, large prevalence studies demonstrating the consequences of comorb

Coronavirus disease 2019 (COVID-19) has spread rapidly from China to other countries around the world, with the World Health Organization characterising it as a global pandemic on 12 March 2020. The number of fatalities owing to COVID-19 is escalating rapidly. COVID-19 is caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), the 7th known human coronavirus. SARS-CoV-2 is assumed to have originated in bats, similar to many other coronaviruses, as it shares 89–96% nucleotide identity with bat coronaviruses. Similar to SARS and Middle East respiratory syndrome (MERS), it is believed SARS-CoV-2 moved from bats to an intermediate host and then to humans. SARS-CoV-2 infection is triggered by viral surface spike protein binding to the human angiotensin-converting enzyme 2 (ACE2) receptor following activation of the spike protein by transmembrane protease serine 2. ACE2 is expressed in the lung (primarily Type II alveolar cells) and tends to be the predominant portal of entry. ACE2 is highly expressed in the heart as well, counteracting the effects of angiotensin II in states with excessive activation of the reninangiotensin system such as hypertension, congestive heart failure and atherosclerosis. There is growing evidence linking COVID-19 to increased morbidity and mortality from cardiovascular disease (CVD).

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