Evaluation of blood pressure variation in recovered COVID-19 patients at one-year follow-up: a retrospective cohort study.

BACKGROUND: Coronavirus disease 2019 (COVID-19) has various sequelae, one of which might be hypertension. We aimed to evaluate COVID-19's impact on blood pressure (BP) in non-hospitalized patients at one-year follow-up. METHOD: A total of 7,950 consecutive COVID-19 patients regularly visiting our cardiology clinic were retrospectively screened. Patients' electronic medical records including demographics, comorbidities, vital signs, treatments, and outcomes, were reviewed by two physicians. Individuals with at least one BP measurement in the three months preceding COVID-19 and one measurement in 12 months or more following recovery were included. BP levels before and after COVID-19 were compared using the paired t-test. RESULTS: 5,355 confirmed COVID-19 patients (mean age 55.51 ± 15.38 years) were included. Hypertension (56.9%) and diabetes mellitus (34%) were the predominant comorbidities, and 44.3% had prior major adverse cardiovascular events. Both systolic (126.90 ± 20.91 vs. 139.99 ± 23.94 mmHg, P < 0.001) and diastolic BP (80.54 ± 13.94 vs. 86.49 ± 14.40 mmHg, P < 0.001) were significantly higher post-COVID-19 vs. pre-COVID-19. Notably, 456 (14%) hypertensive patients experienced exacerbated hypertension, while 408 (17%) patients developed new-onset hypertension, overall 864 (16%) of patients had exacerbation or new hypertension. Linear regression analysis revealed that advanced age, smoking, previous cardiovascular events, hypertension, and diabetes mellitus predict increased BP following COVID-19 (P < 0.001). CONCLUSION: COVID-19 raised systolic and diastolic BP in the long term in non-hospitalized patients, with over one-sixth developing new-onset or exacerbated hypertension. All patients should be evaluated regarding BP, following COVID-19 recovery, particularly those with the mentioned predictive factors. (clinicaltrial.gov: NCT05798208).

Guarding the heart: How SGLT-2 inhibitors protect against chemotherapy-induced cardiotoxicity: SGLT-2 inhibitors and chemotherapy-induced cardiotoxicity.

The introduction of chemotherapy agents has significantly transformed cancer treatment, with anthracyclines being one of the most commonly used drugs. While these agents have proven to be highly effective against various types of cancers, they come with complications, including neurotoxicity, nephrotoxicity, and cardiotoxicity. Among these side effects, cardiotoxicity is the leading cause of morbidity and mortality, with anthracyclines being the primary culprit. Chemotherapy medications have various mechanisms that can lead to cardiac injury. Hence, numerous studies have been conducted to decrease the cardiotoxicity of these treatments. Combination therapy with beta-blockers, Angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers have effectively reduced such outcomes. However, a definitive preventive strategy is yet to be established. Meanwhile, sodium-glucose co-transporter-2 (SGLT-2) inhibitors lower blood glucose levels in type 2 diabetes by reducing its re-absorption in the kidneys. They are thus considered potent drugs for glycemic control and reduction of cardiovascular risks. Recent studies have shown that SGLT-2 inhibitors are crucial in preventing chemotherapy-induced cardiotoxicity. They enhance heart cell viability, prevent degenerative changes, stimulate autophagy, and reduce cell death. This drug class also reduces inflammation by inhibiting reactive oxygen species and inflammatory cytokine production. Moreover, it can not only reverse the harmful effects of anticancer agents on the heart structure but also enhance the effectiveness of chemotherapy by minimizing potential consequences on the heart. In conclusion, SGLT-2 inhibitors hold promise as a therapeutic strategy for protecting cancer patients from chemotherapy-induced heart damage and improving cardiovascular outcomes.

The effect of calcium and vitamin D supplements on blood pressure in postmenopausal women: myth or reality?

Hypertension is a highly prevalent disease with serious cardiovascular and renal complications. Many studies have demonstrated a weak correlation between the consumption of calcium (or calcium plus vitamin D) and blood pressure, suggesting that calcium supplements might reduce blood pressure. However, the results to date remain controversial. In this study, we assessed the effect of calcium and vitamin D supplementation on the blood pressure of postmenopausal women with hypertension as a population group in which the use of calcium supplements is prevalent. This triple-blind randomized clinical trial enrolled 98 women of postmenopausal age with hypertension in 2019. The study period was 8 weeks with close follow-up. We used 24-h ambulatory blood pressure monitoring to record the initial and final blood pressure in all participants. The changes in both the mean systolic (p = 0.047) and diastolic blood pressure (p = 0.015) were suggestive of an increase in blood pressure after consuming calcium and vitamin D supplements. Among patients who had been using calcium channel blockers, calcium and vitamin D supplementation caused a notable increase compared to baseline systolic (p = 0.019) and diastolic blood pressures (p = 0.001). The present results differ from those of previous studies. This suggests that calcium supplementation for postmenopausal women with hypertension requires the close observation of blood pressure to prevent any further increase, especially in women who are being treated with calcium channel blockers (clinicaltrial.gov registration: NCT04618952).

Effects of High- or Moderate-intensity Rosuvastatin on 1-year Major Adverse Cardiovascular Events Post-percutaneous Coronary Intervention.

Background: Although statins decrease mortality in coronary artery disease, the effect of high-dose statins and duration of therapy post-percutaneous coronary intervention (PCI) is not well addressed. Aim: To determine the effective dose of statin to prevent major adverse cardiovascular events (MACEs), such as acute coronary syndrome, stroke, myocardial infarction, revascularisation and cardiac death, after PCI in patients with chronic coronary syndrome. Methods: In this randomised, double-blind clinical trial, all chronic coronary syndrome patients with a recent history of PCI were randomly divided into two groups after 1 month of high-dose rosuvastatin therapy. Over the next year, the first group received rosuvastatin 5 mg daily (moderate intensity), while the second received rosuvastatin 40 mg daily (high intensity). Participants were evaluated in terms of high-sensitivity C-reactive protein and MACEs. Results: The 582 eligible patients were divided into group 1 (n=295) and group 2 (n=287). There was no significant difference between the two groups in terms of sex, age, hypertension, diabetes, smoking, previous history of PCI or history of coronary artery bypass grafting (p>0.05). There were no statistically significant differences in MACE and high-sensitivity C-reactive protein after 1 year between the two groups (p=0.66). Conclusion: The high-dose group had lower LDL levels. However, given the lack of association between high-intensity statins and MACEs in the first year after PCI among chronic coronary syndrome patients, the use of moderate-intensity statins may be as effective as high-intensity statins, and treatment based on LDL targets may suffice.