SGLT2-inhibitors effects on the coronary fibrous cap thickness and MACEs in diabetic patients with inducible myocardial ischemia and multi vessels non-obstructive coronary artery stenosis.

BACKGROUND: Sodium-glucose transporter 2 inhibitors (SGLT2-I) could modulate atherosclerotic plaque progression, via down-regulation of inflammatory burden, and lead to reduction of major adverse cardiovascular events (MACEs) in type 2 diabetes mellitus (T2DM) patients with ischemic heart disease (IHD). T2DM patients with multivessel non-obstructive coronary stenosis (Mv-NOCS) have over-inflammation and over-lipids' plaque accumulation. This could reduce fibrous cap thickness (FCT), favoring plaque rupture and MACEs. Despite this, there is not conclusive data about the effects of SGLT2-I on atherosclerotic plaque phenotype and MACEs in Mv-NOCS patients with T2DM. Thus, in the current study, we evaluated SGLT2-I effects on Mv-NOCS patients with T2DM in terms of FCT increase, reduction of systemic and coronary plaque inflammation, and MACEs at 1 year of follow-up. METHODS: In a multi-center study, we evaluated 369 T2DM patients with Mv-NOCS divided in 258 (69.9%) patients that did not receive the SGLT2-I therapy (Non-SGLT2-I users), and 111 (30.1%) patients that were treated with SGLT2-I therapy (SGLT2-I users) after percutaneous coronary intervention (PCI) and optical coherence tomography (OCT) evaluation. As the primary study endpoint, we evaluated the effects of SGLT2-I on FCT changes at 1 year of follow-up. As secondary endpoints, we evaluated at baseline and at 12 months follow-up the inflammatory systemic and plaque burden and rate of MACEs, and predictors of MACE through multivariable analysis. RESULTS: At 6 and 12 months of follow-up, SGLT2-I users vs. Non-SGLT2-I users showed lower body mass index (BMI), glycemia, glycated hemoglobin, B-type natriuretic peptide, and inflammatory cells/molecules values (p < 0.05). SGLT2-I users vs. Non-SGLT2-I users, as evaluated by OCT, evidenced the highest values of minimum FCT, and lowest values of lipid arc degree and macrophage grade (p < 0.05). At the follow-up end, SGLT2-I users vs. Non-SGLT2-I users had a lower rate of MACEs [n 12 (10.8%) vs. n 57 (22.1%); p < 0.05]. Finally, Hb1Ac values (1.930, [CI 95%: 1.149-2.176]), macrophage grade (1.188, [CI 95%: 1.073-1.315]), and SGLT2-I therapy (0.342, [CI 95%: 0.180-0.651]) were independent predictors of MACEs at 1 year of follow-up. CONCLUSIONS: SGLT2-I therapy may reduce about 65% the risk to have MACEs at 1 year of follow-up, via ameliorative effects on glucose homeostasis, and by the reduction of systemic inflammatory burden, and local effects on the atherosclerotic plaque inflammation, lipids' deposit, and FCT in Mv-NOCS patients with T2DM.

Late Onset Occurrence of Concomitant Myocardial Infarction and Ischemic Stroke in Hospitalized COVID-19 Patient: A Case Report.

We described the case of a 68-year-old COVID-19 patient with hypertension and dyslipidemia who discontinued the cardiovascular medications during hospitalization and experienced a late onset occurrence of concomitant ST-elevation myocardial infarction and ischemic stroke at resolution of SARS-CoV-2 pneumonia.

Prognostic value of combined target-organ damage in patients with essential hypertension.

BACKGROUND: Whether the combination of chronic kidney disease (CKD) and left ventricular hypertrophy (LVH) affects the cardiovascular (CV) risk in patients with uncomplicated hypertension is poorly investigated. The aim of this study was to assess the effects of LVH, CKD, and their combination on CV events in hypertension. METHODS: This study analyzed 1,078 patients with essential hypertension. RESULTS: LVH was present in 104 (9.6%) patients, CKD was present in 556 (51.5%) patients, and the combination of LVH and CKD was found in 174 (16.1%) patients. During the follow-up (median = 84 months), 52 CV events were observed (0.64 events/100 patient-years): 6 (2.4%) in patients without target-organ damage (TOD), 6 (5.7%) in patients with LVH, 20 (3.6%) in patients with CKD, and 20 (11.4%) in patients with combined LVH+CKD. Adjusted hazard ratio (HR) for CV events was 1.62 (P = 0.34) for LVH, 0.951 (P = 0.94) for CKD, and 2.45 (P = 0.03) for LVH+CKD. After multivariable Cox proportional hazard analysis, the combination of LVH+CKD was significantly associated with risk of CV events, when the model was adjusted for sex and age (HR = 2.447; P = 0.03) and for the presence of 1 CV risk factor (HR = 3.226; P = 0.02). In contrast, the association of LVH+CKD was no longer significant when the model was adjusted for sex, age, and the presence of ≥ 2 CV risk factors. CONCLUSIONS: The results of this study highlight the relevance of the interactions between TODs and hemodynamic, anthropometric, and metabolic abnormalities in the CV risk stratification of patients with essential hypertension.

Successful obstetric management of arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic myocardial disorder characterized by the replacement of myocardium by fibro-adipose tissue. The proper obstetric management of this disease remains unclear due to the lack of an adequate number of cases reported in the literature. We report the successful management of a pregnant patient with ARVC. A female patient with ARVC presented to our hospital at 9 weeks of gestation. Before pregnancy, she was treated with bisoprolol, which resulted in a reduction in extrasystoles and she never developed palpitations. Periodical cardiological examinations showed clinical stability, and the only therapeutic change consisted of an increase in the bisoprolol dosage. She delivered at term by elective cesarean section. We decided that avoiding changes in the chronic therapy of our patient was the best management because she had reached clinical stability before pregnancy and discontinuation of therapy may pose an addition risk. In our opinion, cesarean section was the best mode of delivery in our ARVC patient to avoid the stress of labor, which may raise heart rate and cause arrhythmia. Our experience and the case reports in the literature suggest that pregnancy is tolerated in female patients with ARVC, but they need to be monitored during pregnancy by a multidisciplinary team.

Aortic valve sclerosis in patients with peripheral and/or coronary arterial disease.

BACKGROUND: Aortic valve sclerosis (AVS) is a marker of cardiovascular risk; its prevalence increases in elderly and in patients with hypertension and/or coronary arterial disease (CAD). There are no data available in patients with peripheral arterial disease (PAD) and with both CAD and PAD. METHODS: To investigate the presence of AVS, 57 patients with stable CAD, 38 with PAD, and 62 with CAD + PAD where studied by echocardiography. RESULTS: The prevalence of AVS progressively increased within groups (P = 0.005). The prevalence of AVS in PAD doubled that in CAD group (42.1% vs. 22.8%, P < 0.05). PAD patients had a 4.634 (95% CI: 1.02-17.88; P = 0.026) fold increased risk of AVS compared to CAD. Also CAD + PAD group had a higher prevalence of aortic sclerosis when compared to CAD group (50.8% vs. 22.8%, P = 0.001). CAD + PAD showed a 3.799 (95% CI: 1.26-11.45; P < 0 .01) fold greater risk of aortic sclerosis than CAD group. There were no differences in AVS prevalence between CAD + PAD and PAD group (50.8% vs. 42.1%; P = 0.36). Age was related to AVS in both analysis (PAD vs. CAD and CAD + PAD vs. CAD: OR = 1.09, 95% CI: 1.02-1.16, P = 0.011 and OR = 1.13, 95% CI: 1.07-1.21; P < 0.001) but no classical cardiovascular risk factors. CONCLUSIONS: PAD patients have an elevated prevalence of AVS greater than CAD patients. In patients with both disease, the prevalence of AVS is similar to that of patients with PAD alone.

Myocardial fibrosis and diastolic dysfunction in patients on chronic haemodialysis.

BACKGROUND: Left ventricular (LV) diastolic dysfunction is linked to myocardial collagen content in many cardiac diseases. There are no data regarding such relationship in patients with end-stage renal disease (ESRD) undergoing haemodialysis. METHODS: Twenty-five patients with ESRD undergoing haemodialysis were studied by echocardiography. LV diastolic function was investigated by Doppler echocardiography, by analysing LV filling velocities at rest and during loading manoeuvres, which represent an estimate of LV filling pressure. According to the Doppler pattern, LV filling pressure in a given patient was judged to be normal or slightly increased or to be moderately or severely increased. The presence of myocardial fibrosis was estimated by ultrasound tissue characterization with integrated backscatter, which in diastole correlates with the collagen content of the myocardium. RESULTS: Integrated backscatter was higher in patients with moderate or severely increased than in patients with normal or slightly increased LV filling pressure (integrated backscatter: 51.0 +/- 9.8 vs 41.6 +/- 5.6%; P = 0.008). Integrated backscatter was a strong and independent determinant of diastolic dysfunction (odds ratio = 1.212; P = 0.040). CONCLUSION: Our data support the hypothesis that, in a selected population of patients with ESRD undergoing haemodialysis, myocardial fibrosis is associated with LV diastolic myocardial properties.

Thrombosis of mechanical valve prosthesis in patient with recent Caesarean delivery.

We present a case of a mechanical mitral valve thrombosis in a 37-year-old woman occurred 2 days after a Caesarean delivery. The patient stopped warfarin and initiated low-molecular-weight heparin 1 week before the programmed delivery. Subsequently the diagnosis of thrombosis, heparin infusion was started however unsuccessfully and eventually patient was referred for cardiac surgery.