Ranolazine is a medication that inhibits the late phase of the inward sodium current in ventricular myocardial cells, reducing intracellular calcium overload and associated diastolic contractile dysfunction. This effect is particularly beneficial in ventricular tachycardia/fibrillation, premature ventricular beats, and ICD interventions. In patients with ventricular arrhythmias, ranolazine has been shown to significantly shorten QTc intervals and reduce the burden of ventricular tachycardia. Eccentric hypertrophy is the most common remodeling phenotype of HFrEF, involving the lengthening of myocardium. This review compiles clinical evidence investigating the antiarrhythmic properties of ranolazine, focusing primarily on ventricular tachycardia (VT) and atrial fibrillation. Ventricular remodeling following myocardial infarction (MI) involves both ischemic and nonischemic myocardium, and it encompasses two stages. Adverse ventricular remodeling after MI is a process of regional and global structural and functional changes in the heart due to the loss of viable myocardium. Post-infarction HF is mostly caused by adverse remodeling of the left ventricle (LV), a series of molecular, cellular, and interstitial changes.
What are the 4 types of ventricles?
The cerebral ventricular system consists of four ventricles, including two lateral ventricles in each cerebral hemisphere, a third ventricle in the diencephalon, and the fourth ventricle in the hindbrain. It is connected to the central canal of the spinal cord and contains cerebrospinal fluid (CSF), produced by specialized ependymal cells of the choroid plexus. CSF circulates through the ventricular system and returns to the circulation through arachnoid granulations.
The lateral ventricle is a C-shaped cavity within each cerebral hemisphere, lined by ependyma and filled with CSF. It communicates with the third ventricle through the interventricular foramen of Monro. Each ventricle has a central part and three horns: anterior, posterior, and inferior. The central part lies within the parietal lobe and extends from the interventricular foramen to the splenium of the corpus callosum.
What are the types of ventricular remodeling?
Ventricular remodeling, an aspect of cardiomyopathy, involves changes such as ventricular hypertrophy, ventricular dilation, and cardiomegaly. It is primarily influenced by the cardiac myocyte, with other cells such as fibroblasts, collagen, the interstitium, and coronary vessels playing a lesser role. Post-myocardial infarction, myocardial necrosis and disproportionate thinning of the heart can lead to dilatation of the chamber.
The initial remodeling phase may improve LV function and cardiac output, but over time, the heart becomes less elliptical and more spherical, leading to increased ventricular mass and volume, adversely affecting cardiac function.
Cardiac myocyte death can be triggered by necrosis, apoptosis, or autophagy, leading to thinning of the cardiac wall. Survivors of cardiac myocytes can either arrange parallel or in series, contributing to ventricular dilatation or hypertrophy. Reduced expression of V1 myosin and L-type calcium channels on cardiac myocytes is also thought to cause cardiac remodeling.
Fatty acid accounts for 60 to 90 percent of the heart’s energy supply. Post-MI, decreased fatty acid oxidation leads to reduced energy supply for cardiac myocytes, accumulation of fatty acids to toxic levels, and mitochondria dysfunction. This leads to increased oxidative stress on the heart, causing fibroblast proliferation, activation of metalloproteinases, and apoptosis. Inflammatory immune response also contributes to these changes.
What are the 4 types of ventricular arrhythmias?
Ventricular arrhythmias are abnormal heartbeats originating in the lower heart chambers, called ventricles. These arrhythmias cause the heart to beat too fast, preventing oxygen-rich blood from circulating to the brain and body, and may result in cardiac arrest. Stanford Cardiac Arrhythmia Service offers advanced ablation techniques for ventricular arrhythmias, including hybrid surgical-catheter ablation, a minimally invasive procedure that treats the heart on both the inner and outer surface. The program is one of the few in the country offering this advanced treatment.
What is right ventricular remodeling?
The pathophysiology of right ventricular (RV) remodeling is a complex process that includes changes in geometry, wall thickness, and ventricular pressure-volume relationships. It also involves an increase in myocyte dimensions and number, and modifications to the myocardial extracellular matrix and biochemical milieu. RV remodeling has been linked to diseases like pulmonary hypertension, lung transplant, LV pathology, Chagas’ disease, and arrhythmogenic right ventricular cardiomyopathy.
Disease progression may lead to further RV changes, including hypertrophy, dilatation, and alterations in RV hemodynamic status. Multiple methods to assess RV hypertrophy include cine magnetic resonance imaging and 3-D echocardiography, each offering different precision in evaluating RV dimensions and functional performance characteristics. Strategies to prevent RV remodeling include pharmacological agents like vasodilators and angiotensin-converting enzyme inhibitors, as well as more invasive interventions like ventricular assist devices.
What is the right ventricular area change?
The fractional area change is a two-dimensional measure of right ventricular global systolic function, obtained from the apical four-chamber view. It is calculated as the difference in end-diastolic and end-systolic area divided by the end-diastolic area. This measure is crucial in understanding the anatomy, echocardiography, and normal right ventricular dimensions. Studies have shown that the fractional area change can be used to analyze contractile function in the canine right ventricle.
Which of the following is a definition of ventricular remodeling?
Ventricular remodeling, a maladaptive process affecting left ventricular (LV) geometry, mass, and volume, is a significant predictor of morbidity and mortality in patients with heart failure or myocardial infarction. Two classes of drugs, angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic blockers, have been found to inhibit LV remodeling. ACE inhibitors improve survival and prevent progressive remodeling, while beta-adrenergic blockers have a beneficial effect on both survival and remodeling.
The renin-angiotensin system and possibly the sympathetic nervous system play a role in this process. Therefore, ACE inhibitors and beta-blockers should be part of the pharmacologic regimen for treating patients with LV dysfunction to prevent progressive remodeling.
What is the structure of the 4 ventricle?
The fourth ventricle is a diamond-shaped cavity located dorsally to the pons and upper medulla oblongata, anterior to the cerebellum. It is connected to the third ventricle and central canal, and communicates with subarachnoid space through the medial aperture of the foramen of Magendie. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including those for text and data mining, AI training, and similar technologies.
Which of the following are features of ventricles?
The ventricles have thicker walls than the atria and generate higher blood pressures due to the physiological load of pumping blood throughout the body and lungs. The left ventricle has thicker walls than the right ventricle, as it pumps blood to most of the body, while the right ventricle fills only the lungs. The inner walls of the ventricles are covered by irregular muscular columns called trabeculae carneae, which have three types.
The third type, the papillary muscles, originate at their apices at the chordae tendinae, which attach to the cusps of the tricuspid and mitral valves. The left ventricle’s mass, estimated by magnetic resonance imaging, averages 143 g ± 38. 4 g.
What are the mechanisms of ventricular remodeling?
Pathological ventricular remodeling is a complex process influenced by various factors, including ischemia/reperfusion, excessive mechanical load, and cellular processes. These processes include cardiomyocyte loss through cell death pathways, hypertrophic cardiomyocytes, accumulation of excess extracellular matrix, metabolic derangements, insulin resistance, lipotoxicity, and structural changes leading to a pro-arrhythmic phenotype.
Current therapies, such as angiotensin converting enzyme inhibitors, angiotensin receptor blockers, aldosterone antagonists, and β-blockers, have shown significant efficacy in reducing morbidity and mortality in patients with chronic systolic heart failure. However, disease progression continues unabated, and less is known about the proportion of disease where systolic performance of the left ventricular ejection fraction (LV) is preserved.
The majority of current therapies target HFrEF, previously termed systolic heart failure, but it is estimated that 50 of heart failure patients have a preserved left ventricular ejection fraction (HFpEF). Initial studies attributed HFpEF to dysfunction of the myocardium during the filling phase of the cardiac cycle, but it is clear that in some cases, the left ventricular myocardium is an innocent bystander, manifesting dysfunctional filling due to volume overload, insufficiency of perfusion, or inadequate filling times. In many cases, a combination of perturbed diastolic relaxation and excessive volume due to extrinsic factors may combine to perturb ventricular filling.
What causes ventricular Remodelling?
Heart remodeling can occur due to various heart diseases or cardiac damage, such as a heart attack. Initial remodelling occurs immediately after a heart attack to compensate for damage and pump enough blood to the body. If it persists for a long time, it can lead to heart failure. Physiological remodeling occurs during exercise and pregnancy, while pathological remodeling occurs due to heart problems causing pressure overload.
The extent of damage caused by ventricular remodeling can be measured using imaging studies like MRI scans and echocardiography, and left ventricular ejection fraction (LVEF) to measure the amount of blood pumped out of the left ventricle.
Add comment