Pathophysiology, Diagnosis, and Management of Coronary No-Reflow Phenomenon

Coronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but they have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.

Effects of Levosimendan Preconditioning on Left Ventricular Remodeling after Myocardial Reperfusion in Acute Myocardial Infarction Patients Receiving Percutaneous Coronary Intervention

Objective: Levosimendan is a novel drug often used to treat heart failure. We aimed to explore the effects of levosimendan preconditioning on left ventricular remodeling (LVR) after myocardial reperfusion in acute myocardial infarction (AMI) patients receiving the percutaneous coronary intervention (PCI). Methods: A total of 258 AMI patients treated from January 2018 to September 2020 were randomly divided into control and observation groups. Based on conventional drug therapy, levosimendan was given 30 min before PCI for the observation group, and dobutamine was intravenously injected for the control group. Baseline data, thrombolysis in myocardial infarction (TIMI) blood flow grade, myocardial injury markers, and LVR indices were compared, and the influencing factors for LVR were analyzed. Results: After treatment, various degrees of blood perfusion were found, and the TIMI grade was better than that before treatment in both groups (P < .05). The levels of aspartate aminotransferase, creatine kinase-MB, cardiac troponin T, and brain natriuretic peptide (BNP) declined in both groups, more significantly in the observation group (P < .05). Left ventricular end-systolic diameter, left ventricular end-diastolic diameter and left ventricular end-diastolic volume declined, whereas left ventricular ejection fraction rose in both groups, more significantly in the observation group (P < .05). Age and BNP were risk factors for LVR, whereas levosimendan preconditioning was a protective factor (P < .05). Conclusion: Levosimendan preconditioning can protect cardiac function and promote the recovery of the left ventricular structure. Age and BNP are risk factors for LVR after myocardial reperfusion in AMI patients undergoing PCI, and levosimendan preconditioning is a protective factor.

The Effects of Fish Oil on Cardiovascular Diseases: Systematical Evaluation and Recent Advance

Fish oil is rich in unsaturated fatty acids, i.e., eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), both of which are widely distributed in the body such as heart and brain. In vivo and in vitro experiments showed that unsaturated fatty acids may have effects of anti-inflammation, anti-oxidation, protecting vascular endothelial cells, thrombosis inhibition, modifying autonomic nerve function, improving left ventricular remodeling, and regulating blood lipid. Given the relevance to public health, there has been increasing interest in the research of potential cardioprotective effects of fish oil. Accumulated evidence showed that fish oil supplementation may reduce the risk of cardiovascular events, and, in specific, it may have potential benefits in improving the prognosis of patients with hypertension, coronary heart disease, cardiac arrhythmias, or heart failure; however, some studies yielded inconsistent results. In this article, we performed an updated systematical review in order to provide a contemporary understanding with regard to the effects of fish oil on cardiovascular diseases.

Attenuation of Adverse Postinfarction Left Ventricular Remodeling with Empagliflozin Enhances Mitochondria-Linked Cellular Energetics and Mitochondrial Biogenesis

Sodium–glucose cotransporter 2 (SGLT2) inhibitors such as empagliflozin are known to reduce the risk of hospitalizations related to heart failure irrespective of diabetic state. Meanwhile, adverse cardiac remodeling remains the leading cause of heart failure and death in the USA. Thus, understanding the mechanisms that are responsible for the beneficial effects of SGLT2 inhibitors is of the utmost relevance and importance. Our previous work illustrated a connection between adverse cardiac remodeling and the regulation of mitochondrial turnover and cellular energetics using a short-acting glucagon-like peptide-1 receptor agonist (GLP1Ra). Here, we sought to determine if the mechanism of the SGLT2 inhibitor empagliflozin (EMPA) in ameliorating adverse remodeling was similar and/or to identify what differences exist, if any. To this end, we administered permanent coronary artery ligation to induce adverse remodeling in wild-type and Parkin knockout mice and examined the progression of adverse cardiac remodeling with or without EMPA treatment over time. Like GLP1Ra, we found that EMPA affords a robust attenuation of PCAL-induced adverse remodeling. Interestingly, unlike the GLP1Ra, EMPA does not require Parkin to improve/maintain mitochondria-related cellular energetics and afford its benefits against developing adverse remodeling. These findings suggests that further investigation of EMPA is warranted as a potential path for developing therapy against adverse cardiac remodeling for patients that may have Parkin and/or mitophagy-related deficiencies.

GENDER FEATURES OF STRUCTURAL-GEOMETRIC REMODELING OF THE LEFT VENTRICLE IN PATIENTS WITH MYOCARDIAL INFARCTION WITHOUT ELEVATION OF ST SEGMENT

Recently, there has been a tendency to increase the incidence of myocardial infarction without elevation of the ST segment, which, according to some data, accounts for about half of all registered MI. The main problem with this type of infarction is that the long-term prognosis in these patients remains unsatisfactory, and mortality one year after the catastrophe is equal to or even higher than mortality from ST-segment elevation myocardial infarction, which encourages continued predictors of unfavorable prognosis. Objective: to determine the gender characteristics of the structural and geometric remodeling of the left ventricle in patients with myocardial infarction without ST segment elevation. Materials and methods. We conducted a comprehensive study of 200 patients with acute myocardial infarction without ST-segment elevation (NSTEMI) aged 38 to 80 (mean 62.0 ± 0.71, median 62 and interquartile range 55 and 70). The structural and functional state of the myocardium and types of left ventricular remodeling according to transthoracic echocardiography were studied. Results. Analysis of the obtained data shows that echocardiographic parameters in patients with NSTEMI depending on gender did not reveal significant differences between different groups. The exception was the size of the right atrium, which was significantly higher in the group of men compared to women with comparable values of the size of the right ventricle and the ratio of the size of the left to the right atrium. Analysis of the nature of structural and geometric remodeling of the left ventricle in general by groups showed that almost half of the subjects registered concentric hypertrophy of the left ventricle. Concentric left ventricle remodeling was observed in one third of patients and in other patients - normal geometry and eccentric left ventricle hypertrophy. Thus, it was found that concentric models of left ventricle – concentric hypertrophy and concentric remodeling – were registered in the vast majority of patients with NSTEMI. The latter can be explained by a significant proportion of hypertension which was identified by us in most patients and, of course, contributed to the development of concentric models of left ventricle. Analysis of the nature of structural and geometric remodeling of the left ventricle depending on gender showed that in the group of men, compared with women, there was a significant increase in the incidence of concentric remodeling. At the same time, in women, compared with men, there was a significant increase in cases of more severe types of structural remodeling - concentric and eccentric hypertrophy. Thus, we found that gender differences in echocardiographic parameters in patients with NSTEMI relate exclusively to indicators of structural and geometric remodeling of the left ventricle. Signs of concentric and eccentric left ventricular hypertrophy predominate in women, and indicators of normal geometry and concentric left ventricular remodeling in men. This distribution of types of remodeling indicates a more severe course and unfavorable prognosis of NSTEMI in women.

Early onset left ventricular remodeling in juvenile systemic lupus erythematosus; Insight from 3-dimensional speckle tracking echocardiography

Background Early diagnosis and treatment of myocardial affection in patients with systemic lupus erythematosus (SLE) are crucial. Objectives To evaluate the ventricular systolic function in juvenile-onset systemic lupus erythematosus (j-SLE) patients by 3-D speckle tracking echocardiography (3D-STE) and to determine the predictors of left ventricular (LV) dysfunction if present. Methods Twenty-six SLE patients without heart failure and 21 healthy controls were studied by standard echocardiogram and 3D-STE. Conventional parameters included LV ejection fraction (EF), fractional shortening (FS), and mitral annular plane systolic excursion (MAPSE). Global LV strain (GLS) and global area strain (GAS) were obtained by 3D-STE. Medical records, including diagnosis criteria, duration of disease, and SLE disease activity index (SLEDAI) were evaluated. Results The mean age was similar in patients and controls 11.42 vs 11.48 years p = 0.93. The mean duration of the disease was 1.87 ± 1.02 years and SLEDAI ranged from 0 to 9. By conventional and tissue Doppler imaging echocardiography, only MAPSE was significantly lower in SLE patients compared to controls (14.56 vs 18.46 mm, p < 0.001). By 3D speckle tracking echocardiography, GLS and GAS were significantly reduced in SLE patients compared to controls (−15.07 vs −19.9.4%, −34.6% vs −39.7%, respectively, p < 0.001). Multiple linear regression and ROC analyses indicated that the SLEDAI score was the only predictive factor for the left ventricular remodeling. Conclusions These results indicate that early subclinical LV dysfunction occur in jSLE patients even with normal EF and SLE disease activity might be a potential driver for LV deformation.

Targeting cardiomyocyte proliferation as a key approach of promoting heart repair after injury

Cardiovascular diseases such as myocardial infarction (MI) is a major contributor to human mortality and morbidity. The mammalian adult heart almost loses its plasticity to appreciably regenerate new cardiomyocytes after injuries, such as MI and heart failure. The neonatal heart exhibits robust proliferative capacity when exposed to varying forms of myocardial damage. The ability of the neonatal heart to repair the injury and prevent pathological left ventricular remodeling leads to preserved or improved cardiac function. Therefore, promoting cardiomyocyte proliferation after injuries to reinitiate the process of cardiomyocyte regeneration, and suppress heart failure and other serious cardiovascular problems have become the primary goal of many researchers. Here, we review recent studies in this field and summarize the factors that act upon the proliferation of cardiomyocytes and cardiac repair after injury and discuss the new possibilities for potential clinical treatment strategies for cardiovascular diseases.