Endothelial dysfunction, associated with depressed nitric oxide (NO) bioavailability, is awell-recognized contributor to both accelerated atherogenesis and microvascular complications intype 2 diabetes (DM). However, growing evidence points to the comorbidities-driven endothelialdysfunction within coronary microvessels as a key player responsible for left ventricular (LV)diastolic dysfunction, restrictive LV remodeling and heart failure with preserved ejection fraction(HFpEF), the most common form of heart failure in DM. In this review we have described: (1)multiple cellular pathways which may link depressed NO bioavailability to LV diastolicdysfunction and hypertrophy; (2) hemodynamic consequences and prognostic effects of restrictiveLV remodeling and combined diastolic and mild systolic LV dysfunction on cardiovascularoutcomes in DM and HFpEF, with a focus on the clinical relevance of endothelial dysfunction; (3)novel therapeutic strategies to improve endothelial function in DM. In summary, beyondassociations with accelerated atherogenesis and microvascular complications, endothelialdysfunction supplements the multiple interwoven pathways affecting cardiomyocytes, endothelialcells and the extracellular matrix with consequent LV dysfunction in DM patients. The associationamongst impaired endothelial function, reduced coronary flow reserve, combined LV diastolic anddiscrete systolic dysfunction, and low LV stroke volume and preload reserve—all of which areadverse outcome predictors—is a dangerous constellation of inter-related abnormalities, underlyingthe development of heart failure. Nevertheless, the relevance of endothelial effects of novel drugsin terms of their ability to attenuate cardiovascular remodeling and delay heart failure onset in DMpatients remains to be investigated

Although ECG used to be a traditional method to detect left ventricular hypertrophy (LVH), its importance has decreased over the years and echocardiography has emerged as a routine technique to diagnose LVH. Intriguingly, an independent negative prognostic effect of the “electrical” LVH (i.e., by ECG voltage criteria) beyond echocardiographic LVH was demonstrated both in hypertension and aortic stenosis (AS), the most prevalent heart valve disorder. Our aim was to estimate associations of the ECG-LVH voltage criteria with echocardiographic LVH and indices of AS severity. We retrospectively manually analyzed ECG tracings of 50 patients hospitalized in our center for severe isolated aortic stenosis, including 32 subjects with echocardiographic LVH. The sensitivity of single traditional ECG-LVH criteria in detecting echocardiographic LVH was 9–34% and their respective specificity averaged 78–100%. The ability to predict echocardiographic LVH was higher for S-waves than R-waves (mean area under the receiver operating curve (AUC): 0.62–0.70 vs. 0.58–0.65). Among combinations of R- and S-waves, the discriminating ability was highest for the Cornell voltage (AUC: 0.71) compared to the Sokolow–Lyon, Romhilt and Gubner–Ungerleider voltage (AUC: 0.62–0.68). By multiple regression, peak aortic pressure gradient was positively related to the Sokolow–Lyon (β = 1.7 ± 0.5, p = 0.002) and Romhilt voltage (β = 1.3 ± 0.5, p = 0.01), but not Cornell (0.5 ± 0.3, p = 0.2) or Gubner-Ungerleider voltage (β = 0.0 ± 0.5, p > 0.9), regardless of LV mass index. In conclusion, echocardiographic LVH and stenosis severity appear to have distinct associations with traditional ECG-LVH criteria in AS. A moderate diagnostic superiority of the Cornell voltage criterion with regard to anatomic LVH might result from its unique ability to include depolarization vectors in both the frontal and horizontal plane with consequent lesser sensitivity to the confounding effect of obesity.

Traditional electrocardiographic (ECG) criteria for left ventricular hypertrophy (LVH), introduced in the pre-echocardiographic era of diagnosis, have a relatively low sensitivity (usually not exceeding 25–40%) in detecting LVH. A novel Peguero-Lo Presti ECG-LVH criterion was recently shown to exhibit a higher sensitivity than the traditional ECG-LVH criteria in hypertension. Our aim was to test the diagnostic ability of the novel Peguero-Lo Presti ECG-LVH criterion in severe aortic stenosis. We retrospectively analyzed 12-lead ECG tracings and echocardiographic records from the index hospitalization of 50 patients with isolated severe aortic stenosis (mean age: 77 ± 10 years; 30 women and 20 men). Exclusion criteria included QRS > 120 ms, bundle branch blocks or left anterior fascicular block, a history of myocardial infarction, more than mild aortic or mitral regurgitation, and significant LV dysfunction by echocardiography. We compared the agreement of the novel Peguero-Lo Presti criterion and traditional ECG-LVH criteria with echocardiographic LVH (LV mass index > 95 g/m2 in women and >115 g/m2 in men). Echocardiographic LVH was found in 32 out of 50 study patients. The sensitivity of the Peguero-Lo Presti criterion in detecting LVH was improved (55% vs. 9–34%) at lower specificity (72% vs. 78–100%) in comparison to 8 single traditional ECG-LVH criteria. Additionally, the positive predictive value (77% vs. 72%), positive likelihood ratio (2.0 vs. 1.5), and odds ratio (3.2 vs. 2.4) were higher for the Peguero-Lo Presti criterion versus the presence of any of these 8 traditional ECG-LVH criteria. Cohen’s Kappa, a measure of concordance between ECG and echocardiography with regard to LVH, was 0.24 for the Peguero-Lo Presti criterion, −0.01–0.13 for single traditional criteria, and 0.20 for any traditional criterion. However, by the receiver operating characteristics (ROC) curve analysis, the overall ability to discriminate between patients with and without LVH was insignificantly lower for the Peguero-Lo Presti versus Cornell voltage as a continuous variable (area under the ROC curve: 0.65 (95% CI, 0.48–0.81) vs. 0.71 (0.55–0.86), p = 0.5). In conclusion, our preliminary results suggest a slightly better, albeit still low, agreement of the novel Peguero-Lo Presti ECG criterion compared to the traditional ECG-LVH criteria with echocardiographic LVH in severe aortic stenosis.

Background: Coronary artery perforation (CAP) is a rare but potentially life-threatening complication of percutaneous coronary interventions (PCIs) due to the risk of cardiac tamponade. Strikingly, in contrast to numerous analyses of CAP predictors, only few studies were focused on the predictors of tamponade after PCI, once iatrogenic CAP has occurred. Our aim was to search for clinical and periprocedural characteristics, including the coronary artery involved, associated with the development of acute cardiac tamponade among patients experiencing CAP. Methods: From the medical records of nine centers of invasive cardiology in southern Poland, we retrospectively selected 81 patients (80% with acute myocardial infarction) who had iatrogenic CAP with a visible extravasation jet during angiography (corresponding to type III CAP by the Ellis classification, CAPIII) over a 15-year period (2005–2019). Clinical, angiographic and periprocedural characteristics were compared between the patients who developed acute cardiac tamponade requiring urgent pericardiocentesis in the cathlab (n = 21) and those with CAPIII and without tamponade (n = 60). Results: CAPIII were situated in the left anterior descending artery (LAD) or its diagonal branches (51%, n = 41), right coronary artery (RCA) (24%, n = 19), left circumflex coronary artery (LCx) (16%, n = 13), its obtuse marginal branches (7%, n = 6) and left main coronary artery (2%, n = 2). Acute cardiac tamponade occurred in 24% (10 of 41), 21% (4 of 19) and 37% (7 of 19) patients who experienced CAPIII in the territory of LAD, RCA and LCx, respectively. There were no significant differences in the need for urgent pericardiocentesis (37%) in patients with CAPIII in LCx territory (i.e., the LCx or its obtuse marginal branches) compared to CAPIII in the remaining coronary arteries (23%) (p = 0.24). However, when CAPIII in the LCx were separated from CAPIII in obtuse marginal branches, urgent pericardiocentesis was more frequently performed in patients with CAPIII in the LCx (54%, 7 of 13) compared to subjects with CAPIII in an artery other than the LCx (21%, 14 of 68) (p = 0.03). The direction of this tendency remained consistent regardless of CAP management: prolonged balloon inflation only (n = 26, 67% vs. 13%, p = 0.08) or balloon inflation with subsequent stent implantation (n = 55, 50% vs. 24%, p = 0.13). Besides LCx involvement, no significant differences in other characteristics were observed between patients according to the need of urgent pericardiocentesis. Conclusions: CAPIII in the LCx appears to lead to a higher risk of acute cardiac tamponade compared to perforations involving other coronary arteries. This association may possibly be linked to distinct features of LCx anatomy and/or well-recognized delays in diagnosis and management of LCx-related acute coronary syndromes.