Vikash Jaiswal

Abstract Cardiac amyloidosis is caused by the extracellular deposition of amyloid fibrils in the heart, involving not only the myocardium but also any cardiovascular structure. Indeed, this progressive infiltrative disease also involves the cardiac valves and, specifically, shows a high prevalence with aortic stenosis. Misfolded protein infiltration in the aortic valve leads to tissue damage resulting in the onset or worsening of valve stenosis. Transthyretin cardiac amyloidosis and aortic stenosis coexist in patients > 65 years in about 4–16% of cases, especially in those undergoing transcatheter aortic valve replacement. Diagnostic workup for cardiac amyloidosis in patients with aortic stenosis is based on a multi-parametric approach considering clinical assessment, electrocardiogram, haematologic tests, basic and advanced echocardiography, cardiac magnetic resonance, and technetium labelled cardiac scintigraphy like technetium-99 m (99mTc)-pyrophosphate, 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid, and 99mTc-hydroxymethylene diphosphonate. However, a biopsy is the traditional gold standard for diagnosis. The prognosis of patients with coexisting cardiac amyloidosis and aortic stenosis is still under evaluation. The combination of these two pathologies worsens the prognosis. Regarding treatment, mortality is reduced in patients with cardiac amyloidosis and severe aortic stenosis after undergoing transcatheter aortic valve replacement. Further studies are needed to confirm these findings and to understand whether the diagnosis of cardiac amyloidosis could affect therapeutic strategies. The aim of this review is to critically expose the current state-of-art regarding the association of cardiac amyloidosis with aortic stenosis, from pathophysiology to treatment.

BACKGROUND: COVID-19 was initially considered to be a respiratory illness, but current findings suggest that SARS-CoV-2 is increasingly expressed in cardiac myocytes as well. COVID-19 may lead to cardiovascular injuries, resulting in myocarditis, with inflammation of the heart muscle. OBJECTIVE: This systematic review collates current evidence about demographics, symptomatology, diagnostic, and clinical outcomes of COVID-19 infected patients with myocarditis. METHODS: In accordance with PRISMA 2020 guidelines, a systematic search was conducted using PubMed, Cochrane Central, Web of Science and Google Scholar until August, 2021. A combination of the following keywords was used: SARS-CoV-2, COVID-19, myocarditis. Cohorts and case reports that comprised of patients with confirmed myocarditis due to COVID-19 infection, aged >18 years were included. The findings were tabulated and subsequently synthesized. RESULTS: In total, 54 case reports and 5 cohorts were identified comprising 215 patients. Hypertension (51.7%), diabetes mellitus type 2 (46.4%), cardiac comorbidities (14.6%) were the 3 most reported comorbidities. Majority of the patients presented with cough (61.9%), fever (60.4%), shortness of breath (53.2%), and chest pain (43.9%). Inflammatory markers were raised in 97.8% patients, whereas cardiac markers were elevated in 94.8% of the included patients. On noting radiographic findings, cardiomegaly (32.5%) was the most common finding. Electrocardiography testing obtained ST segment elevation among 44.8% patients and T wave inversion in 7.3% of the sample. Cardiovascular magnetic resonance imaging yielded 83.3% patients with myocardial edema, with late gadolinium enhancement in 63.9% patients. In hospital management consisted of azithromycin (25.5%), methylprednisolone/steroids (8.5%), and other standard care treatments for COVID-19. The most common in-hospital complication included acute respiratory distress syndrome (66.4%) and cardiogenic shock (14%). On last follow up, 64.7% of the patients survived, whereas 31.8% patients did not survive, and 3.5% were in the critical care unit. CONCLUSION: It is essential to demarcate COVID-19 infection and myocarditis presentations due to the heightened risk of death among patients contracting both myocardial inflammation and ARDS. With a multitude of diagnostic and treatment options available for COVID-19 and myocarditis, patients that are under high risk of suspicion for COVID-19 induced myocarditis must be appropriately diagnosed and treated to curb co-infections.

Background A new clinical syndrome has been recognized following the COVID-19 vaccine, termed thrombosis with thrombocytopenia syndrome (TTS). The following systematic review focuses on extrapolating thrombotic risk factors, clinical manifestations, and outcomes of patients diagnosed with TTS following the COVID-19 vaccine. Methods We utilized the World Health Organization's criteria for a confirmed and probable case of TTS following COVID-19 vaccination and conducted a systematic review and posthoc analysis using the PRISMA 2020 statement. Data analysis was conducted using SPSS V25 for factors associated with mortality, including age, gender, anti-PF4/heparin antibodies, platelet nadir, D-dimer peak, time to event diagnosis, arterial or venous thrombi. Results Of the 175 studies identified, a total of 25 studies with 69 patients were included in this systematic review and post hoc analysis. Platelet nadir ( P < .001), arterial or venous thrombi ( χ2 = 41.911, P = .05), and chronic medical conditions ( χ2 = 25.507, P = .041) were statistically associated with death. The ROC curve analysis yielded D-dimer (AUC = .646) and platelet nadir (AUC = .604) as excellent models for death prediction. Conclusion Adenoviral COVID-19 vaccines have been shown to trigger TTS, however, reports of patients having received mRNA COVID-19 vaccines are also present. Healthcare providers are recommended to maintain a high degree of suspicion among individuals who have received the COVID-19 vaccine within the last 4 weeks.

BACKGROUND: The clinical impact of the influenza vaccination on cardiovascular outcomes in people with established cardiovascular disease (CVD) is still debated. AIM: The aim of this meta-analysis was to estimate the effect of influenza vaccination on cardiovascular and cerebrovascular outcomes among patients with established CVD. METHODS: We systematically searched all electronic databases from inception until 15 April 2022. Primary clinical outcomes were all-cause mortality, and major adverse clinical events (MACEs). Secondary endpoints were heart failure, myocardial infarction, cardiovascular mortality, and stroke. RESULTS: Eighteen articles (five randomized trials and thirteen observational studies), with a total of 22 532 165 patients were included in the analysis. There were 217 072 participants included in the high cardiovascular risk or established CVD population (vaccinated n = 111 073 and unvaccinated n = 105 999). The mean age of the patients was 68 years old, without any difference between groups (69 vs. 71) years. At a mean follow-up of 1.5 years, the vaccinated group was associated with a lower risk of all-cause mortality [hazard ratio (HR), 0.71(95% CI, 0.63-0.80), P < 0.001], MACE [HR, 0.83(95% CI:0.72-0.96), P = 0.01], CV mortality [HR, 0.78(95% CI:0.68-0.90), P < 0.001], and MI [HR, 0.82 (95% CI:0.74-0.92), P < 0.001] compared to the unvaccinated group. While the incidence of stroke [HR, 1.03 (95% CI, 0.92-1.06), P = 0.61] and heart failure [HR, 0.74 (95% CI, 0.51-1.08), P = 0.12] did not differ between the two groups. CONCLUSION: Influenza vaccination reduced MACEs, all-cause mortality, CV mortality, and MI. These highlighted the importance of influenza vaccination in established CVD or high cardiovascular risk.

Various studies have suggested the possible cardiovascular (CV) protective effects of the pneumococcal vaccine (PV). Therefore, we conducted a meta-analysis to assess the association between recipients of PV with mortality and CV outcomes among patients with and without established cardiovascular disease. We performed a systematic literature search in PubMed, Embase, and Scopus for studies evaluating the effect of PV on mortality and CV outcomes. A total of 15 studies with 347,444 patients were included in the meta-analysis: 111,784 patients received PV (32%) and 235,660 patients were in the unvaccinated group (68%). Recipients of PV were associated with decreased all-cause mortality (HR, 0.76 (95% CI: 0.66 to 0.87), p < 0.001). PV was associated with a decrease in the incidence of myocardial infarction (MI) (HR, 0.73 (95% CI: 0.56−0.96), p = 0.02), without significant reduction in CV mortality (HR, 0.87 (95% CI: 0.72−1.07), p = 0.18) and stroke (HR, 1.01 (95% CI: 0.93−1.10), p = 0.82). Our study found PV was associated with decreased risk of all-cause mortality and MI. Future RCTs will be necessary to confirm benefits associated with receipt of PV.