Mid-Diastolic Events (L Events): A Critical Review

Mid-diastolic events (L events) include three phenomena appreciable on echocardiography occurring during diastasis: mid-diastolic transmitral flow velocity (L wave), mid-diastolic mitral valve motion (L motion), and mid-diastolic mitral annular velocity (L’ wave). L wave is a known marker of advanced diastolic dysfunction in different pathological clinical settings such as left ventricle and atrial remodeling, overloaded states, and cardiomyopathies. Patients with L events have poor outcomes with a higher risk of developing heart failure symptoms and arrhythmic complications, including sudden cardiac death. The exact mechanism underlying the genesis of mid-diastolic events is not fully understood, just as the significance of these events in healthy young people or their presence at the tricuspid valve level. We also report an explicative case of a patient with L events studied using speckle tracking imaging of the left atrium and ventricle at the same reference heartbeat supporting the hypothesis of a post-early diastolic relaxation or a “two-step” ventricular relaxation for L wave genesis. Our paper seeks to extend knowledge about the pathophysiological mechanisms on mid-diastolic events and summarizes the current knowledge.

Impact of coronary artery tortuosity in ischemic and non-ischemic cardiovascular pathology

The aim of this paper was to review based on the existing literature the impact of coronary artery tortuosity on coronary pathology. Primarily, an attempt was made to establish the implication of coronary tortuosity as a physio-pathological mechanism of inducing ischemia in patients with non-obstructive coronary artery disease (CAD). Because the prevalence of tortuosity is higher in severe hypertensive patients, a second purpose of this paper was to review this association by understanding the physio-pathological processes and fluid dynamics in hypertrophic heart. Particularly, the effect of coronary tortuosity on systolic function with reference to longitudinal function and ventricular relaxation was addressed. Finally, were discussed- the technical difficulties imposed by coronary tortuosity to percutaneous coronary interventions.

Abstract 13502: Impact of Udenafil on Echocardiographic Indices of Single Ventricle Size and Function in Fuel Study Participants

Introduction: The Pediatric Heart Network’s Fontan Udenafil Exercise Longitudinal (FUEL) Trial (Mezzion Pharma Co. Ltd., NCT 02741115) demonstrated improvements in exercise capacity following 6 months of treatment with udenafil (87.5 mg po BID). The effect of udenafil on echocardiographic measures of single ventricle (SV) function in this cohort has not been studied. Methods: Protocol echocardiograms were obtained at baseline and 26 weeks after initiation of udenafil/placebo. Linear regression compared change from baseline in indices of SV systolic, diastolic and global function, atrioventricular valve (AVV) regurgitation and mean Fontan fenestration gradient in the udenafil cohort vs placebo, controlling for ventricular morphology (LV vs. RV/other). Effects of ventricular morphology on echo measures and its interaction over time was also evaluated. Difficult imaging windows limited consistent capture of all measures. Results: The 191 udenafil participants had significantly improved myocardial performance index (p=0.03), AVV inflow peak E and A velocities (p = 0.007 and 0.03), and annular DTI-derived peak e’ velocity (p = 0.008) compared to 195 placebo participants (Table). There were no significant differences in change in SV size, systolic function, AVV regurgitation severity or mean fenestration gradient. Although LV morphology participants had significantly more favorable indices of SV size and function (lower volumes and areas, E/e’ ratio, systolic:diastolic time and AVV regurgitation, and higher annular s’ and e’ velocity) at baseline, there was no differential effect of udenafil by ventricular morphology at 26 weeks. Conclusions: FUEL participants who received udenafil demonstrated a significant improvement in global and diastolic echo indices. The changes in diastolic function suggest improvement in pulmonary venous return and/or augmented ventricular relaxation, which may help explain improved exercise performance in that cohort.

Organ Damage due to Elevation of Blood Pressure on NaCl-induced

Introduction: High salt diet is known to induce or aggravate hypertension in hypertensive rats and humans. The elevation of blood pressure by NaCl-induced promotes cardiac hypertrophy, the impairment of left ventricular relaxation, endothelial dysfunction, and kidney injury. This study aimed to examine whether NaCl-induced caused increase blood pressure and weight of organs. Methods: Eight weeks old male Mus musculus were divided to two groups, one group was given NaCl 8% by intraperitoneal injection for 8 hours.Results: Blood pressure was measured previously, in this study systolic and diastolic blood pressure increased significantly (p < 0.05). The increasing of blood pressure was followed by significant increase in organ weight, such as heart and kidney (p < 0.05). Conclusion: This result suggested that NaCl-induced caused hypertension and increased organs weight that may cause early process of damages in organs.

Effects of myocardial function and systemic circulation on regional coronary perfusion

We present a model of left ventricle perfusion based on an anatomically realistic coronary tree structure that includes its interaction with the systemic circulation. Left ventricular relaxation rate has a significant effect on the regional distribution of coronary flow and myocardial work.