The pandemic SARS coronavirus 2 utilizes efficient mechanisms to establish infection and evade the immune system. Established infection leads to severe inflammation in susceptible patients, the mai...

Ischaemic mitral regurgitation (IMR) is consequence of left ventricular (LV) remodelling after myocardial infarction. In some cases, the mitral valve enlarges to compensate for LV remodelling and tenting, improving its coaptation; a process termed ‘plasticity’. We sought to identify clinical and echocardiographic factors associated with plasticity in patients with chronic inferior myocardial infarction (CII). This study included 91 revascularized CII patients and 46 controls. Plasticity and IMR severity were evaluated by 2D transthoracic echocardiography. Compared with controls, CII patients were older (59 vs. 25 years) and mostly men (80% vs. 46%), both P < 0.001. Chronic inferior myocardial infarction patients also had significant LV remodelling: larger LV volumes, larger mitral tenting areas, larger coaptation depths, longer mitral leaflets and chords, and worse mitral regurgitation (all P ≤ 0.03). Of 91 CII patients, 60 had mitral plasticity (longer anterior and posterior leaflets and longer posterior chords, all P < 0.001), despite not exhibiting significantly larger LV volumes, tenting area or coaptation depth, when compared with patients with no plasticity. Contralateral (anterior) papillary muscle-to-annulus length tended to be increased in CII plasticity patients (P = 0.05). Also they had less moderate and severe IMR (both P < 0.04) compared with non-plasticity CII patients. Multivariate analysis demonstrated independent associations between plasticity and smoking [odds ratio (OR) 0.03, 0.002–0.57; P = 0.019], duration of type-2 diabetes (OR 1.19, 1.007–1.42; P = 0.04) and haemoglobin (OR 2.17, 1.25–3.76; P = 0.005). Mitral plasticity results in less moderate and severe IMR. Longer time-duration of diabetes mellitus and higher haemoglobin level are independently associated with mitral plasticity, while smoking independently associates with no plasticity. Increased anterior papillary muscle-to-annulus length in CII patients with plasticity suggests complex LV remodelling mechanisms are involved in plasticity.

Severe aortic stenosis (AS), leads to pathological left ventricular remodeling that may worsen with concomitant overweight and obesity (OW/O). We aimed to prospectively analyze the impact of OW/O on ventricular remodeling in severe AS, by evaluating the percentage of intraendomyocardial fibrosis (PIEF) and the percentage of infiltrating intraendocardial lipid vacuoles (PIELV) and its relationship to global longitudinal strain (GLS) in patients with OW/O. 44 patients with severe AS were included, 13 non-obese (29%) and 31 OW/O (71%), all of them with left ventricular ejection fraction ≥ 55%. GLS was evaluated with 2D speckle tracking. During valve replacement, an endocardial biopsy was obtained, where PIEF and PIELV were analyzed. Patients with higher PIEF and PIELV had greater body mass index (p < 0.0001) and worse GLS (p < 0.0053). A GLS cut-off point < -14% had a sensitivity of 75%, and a specificity of 92.8% to detect important PIEF (AUC: 0.928, 95% confidence interval: 0.798-1.00). On multivariate analysis, OW/O and PIELV were independently associated to the PIEF, and OW/O and PIEF were independently associated to GLS. A high correlation between the amount of PIELV and PIEF were found. Patients with severe AS and OW/O have greater PIEF and PIELV, suggesting more pathological remodeling. GLS is useful to detect subclinical myocardial injury and is potentially useful for endomyocardial fibrosis detection. The presence of higher PIELF may be a trigger factor for the development of intraendomyocardial fibrosis.

The I/D insertion/deletion polymorphism of the angiotensin-converting enzyme has been related to hypertension. This polymorphism also seems to have gender related implications. Angiotensin II contributes to the production and release of oxygen reactive species that react with nitric oxide, inactivating its effects. To establish whether the ACE I/D polymorphism correlates with nitric oxide plasma metabolites in healthy men and women. Among 896 subjects between 18 and 30 years of age range, 138 fulfilled inclusion criteria. The polymorphism was identified by polymerase chain reaction, and blood nitric oxide metabolites were analyzed following the method described by Bryan. Both systolic and diastolic arterial pressures were higher in men than in women (107/67 vs. 101/65 mm Hg, p<0.001). In terms of the ACE gene, there were differences in the concentration of nitric oxide metabolites in men with the I/D and D/D genotypes when compared to carriers of the I/I genotype (33.55 and 29.23 vs. 53.74 pmol/ml; p=<0.05), while there were no significant differences in women when compared by genotype. Men with the D/D genotype had higher systolic blood pressure than I/D carriers (111 vs. 104 mm Hg, p<0.05). We observed no arterial blood pressure differences in women when grouped by ACE genotype. The ACE D/D genotype was associated with nitric oxide metabolite levels and systolic blood pressure in clinically healthy men while it had no effect in women.

Aortic stenosis is a progressive heart valve disorder characterized by calcification of the leaflets. Heart rate variability (HRV) analysis has been proposed for assessing the heart response to autonomic activity, which is documented to be altered in different cardiac diseases. The objective of the study was to evaluate changes of HRV in patients with aortic stenosis by an active standing challenge. Twenty-two volunteers without alterations in the aortic valve (NAV) and twenty-five patients diagnosed with moderate and severe calcific aortic valve stenosis (AVS) participated in this cross-sectional study. Ten minute electrocardiograms were performed in a supine position and in active standing positions afterwards, to obtain temporal, spectral, and scaling HRV indices: mean value of all NN intervals (meanNN), low-frequency (LF) and high-frequency (HF) bands spectral power, and the short-term scaling indices (α₁ and α_sign1). The AVS group showed higher values of LF, LF/HF and α_sign1 compared with the NAV group at supine position. These patients also expressed smaller changes in meanNN, LF, HF, LF/HF, α_1, and α_sign1 between positions. In conclusion, we confirmed from short-term recordings that patients with moderate and severe calcific AVS have a decreased cardiac parasympathetic supine response and that the dynamic of heart rate fluctuations is modified compared to NAV subjects, but we also evidenced that they manifest reduced autonomic adjustments caused by the active standing challenge.

In recent decades, adults living with congenital heart disease (ACHD) have improved their survival, thus increasing their predisposition to the onset of cardiometabolic risk factors and chronic health conditions. The purpose of this study was to describe cardiometabolic risk profiles in the ACHD population and their relationship to congenital heart disease (CHD) lesion complexity. We performed a cross-sectional study from ACHD in a third-tier referral center in Mexico City. The association between cardiometabolic risk factors and CHD complexity was estimated using logistic regression models. Our study cohort included 1,171 ACHD patients (median age: 31 [IQR: 23.2-42.7] years, male 63.6%). Cardiac diagnosis was classified as mild (44.9%), moderate (37.8%), and severe (17.2%) CHD complexity. Low high-density lipoprotein cholesterol (55%) was the most common cardiometabolic risk factor; followed by insulin resistance (54.5%) and prediabetes (52.4%). Patients with mild and moderate CHD had a higher prevalence of obesity and metabolic syndrome, while patients with severe CHD had a higher prevalence of hyperuricemia and subclinical hypothyroidism. In the logistic regression analysis, the severity of CHD was associated with higher odds of hyperuricemia (moderate CHD, OR: 1.87; 95% CI: 1.20-2.93; P = 0.010; severe CHD, OR: 2.75; 95% CI: 1.64-4.62; P < 0.001) and lower risks of metabolic syndrome (OR: 0.61; 95% CI: 0.41-0.91; P = 0.010), prediabetes (OR: 0.58; 95% CI: 0.42-0.81; P < 0.001), and arterial hypertension (OR: 0.49; 95% CI: 0.33-0.74; P < 0.001) compared with mild CHD complexity. We observed high rates of cardiometabolic risk factors in Mexican ACHD patients and these risk profiles varied by CHD lesion complexity. These results highlight the need for ongoing metabolic health surveillance in the ACHD population.