Opinion - (2022) Volume 6, Issue 3
Received: 06-May-2022, Manuscript No. jigc-22-67051;
Editor assigned: 07-May-2022, Pre QC No. P-67051;
Reviewed: 16-May-2022, QC No. Q-67051;
Revised: 22-May-2022, Manuscript No. R-67051;
, DOI: 10.37421/2684-4591.2022.6.157
Citation: Lederman, Andrew. “Hypertrophic Cardiomyopathy in Patient with Heart Issues.” J Interv Gen Cardiol 6 (2022): 157.
Copyright: © 2022 Lederman A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Hypertrophic cardiomyopathy (HCM) or obstructive hypertrophic cardiomyopathy (HOCM) is a condition in which the heart thickens for no obvious reason. The most commonly affected areas of the heart are the interventricular septum and the ventricles. This reduces the heart's ability to pump blood and may also cause problems with electrical conduction. Patients with HCM may suffer a wide range of symptoms. Weariness, limb edoema, and shortness of breath are some of the symptoms that people may experience. It can also make you pass out or induce chest pain. The symptoms may be aggravated if a person is dehydrated. Heart failure, abnormal heartbeats, and sudden cardiac death are all issues that can occur.
HCM is frequently inherited from one's parents in an a utosomal dominant manner. Mutations in genes involved in the generation of heart muscle proteins are frequently the cause. Genetic causes of left ventricular hypertrophy include Fabry disease, Friedreich's ataxia, and specific medicines like tacrolimus. Another cause of an enlarged heart could be an athlete's heart or hypertension (high blood pressure). HCM is diagnosed using a family history or pedigree, an ECG, an echocardiogram, and stress testing. There is also the option of genetic testing. HCM is distinct from other inherited types of cardiomyopathy because it is autosomal dominant, whereas Fabry disease is X-linked and Friedreich's Ataxia is autosomal recessive.
Treatment may be influenced by symptoms and other risk factors. Disopyramide and beta blockers are two drugs that may be used. An implantable cardiac defibrillator may be recommended for patients with certain types of irregular heartbeats. If alternate treatments don't work, surgery, such as a septal myectomy or a heart transplant, may be required. With treatment, the chance of dying from the disease is less than 1% each year.
Signs and symptoms
HCM can be brought on by a number of reasons. Many people with HCM are asymptomatic or have only minor symptoms, and many people with HCM disease genes do not have clinically visible disease. Shortness of breath due to stiffening and decreased blood filling of the ventricles, exertional chest pain (also known as angina) due to reduced blood flow to the coronary arteries, unpleasant awareness of the heart beat (palpitations), as well as disruption of the electrical system running through the abnormal heart muscle, lightheadedness, weakness, fainting, and sudden cardiac death are all symptoms of HCM.
Shortness of breath is primarily caused by the stiffness of the left ventricle (LV), which not only prevents ventricular filling but also leads to increased pressure in the left ventricle and left atrium, resulting in back pressure and interstitial congestion in the lungs. Symptoms are unaffected by the presence or severity of an outflow tract gradient. The symptoms (particularly exercise intolerance and dyspnea) are similar to those of congestive heart failure, but the treatment is different. Beta blockers are used in both cases, however diuretics, a popular CHF treatment, exacerbate symptoms in hypertrophic obstructive cardiomyopathy by lowering ventricular preload volume and thereby increasing outflow resistance (less blood to push aside the thickened obstructing tissue).
The diagnosis of hypertrophic cardiomyopathy is based on a variety of aspects of the disease process. While echocardiography, cardiac catheterization, and cardiac MRI are used to diagnose the disease, ECG, genetic testing (albeit not primarily for diagnosis), and any family history of HCM or unexplained sudden death in otherwise healthy people are also important factors to examine. According to cardiac MRI, the bottom part of the ventricular septum thickens more than 15 mm in 60 to 70% of cases. T1- weighted imaging can detect scarring in cardiac tissues, whereas T2-weighted imaging can detect oedema and inflammation, both of which are connected to acute symptoms including chest pain and fainting.
Despite the fact that HCM might be asymptomatic, those who are affected can develop symptoms ranging from mild to severe heart failure and sudden cardiac death at any age, from infancy to old age. In the United States, HCM is the most common genetic cardiovascular disease and the leading cause of sudden cardiac death in young athletes. According to one study, since 1982, when routine cardiac screening for athletes was started, the rate of sudden cardiac mortality in young competitive athletes in the Veneto area of Italy has fallen by 89 percent, from an abnormally high beginning rate. However, studies show that, as of 2010, the rate of sudden cardiac death among all HCM patients had dropped to less than 1%. Those who have received a positive test.
An echocardiogram (ECHO), which can be followed by an electrocardiogram (ECG) to look for heart abnormalities, can diagnose HCM with an accuracy of 80% or higher. Cardiac Magnetic Resonance Imaging (CMR), the gold standard for analysing the physical features of the left ventricle wall, can be employed as an alternative screening method when an echocardiogram provides unclear data. For example, segmental lateral ventricular hypertrophy cannot be detected just using echocardiography. In children under the age of thirteen, left ventricular hypertrophy may or may not exist. This puts doubt on pre-adolescent echocardiography results.
Researchers employed CMR to investigate asymptomatic carriers of an HCM-causing mutation and discovered crypts in the interventricular septal tissue. The formation of these crypts has been considered as an indication of myocyte disorganisation and altered vessel walls, which could lead to the clinical manifestation of HCM in the future. One possible explanation is that most family history research focuses primarily on whether or not there was a sudden death. It disregards the age of relatives who died of sudden cardiac death, as well as the frequency with which they perished.
Many people with hypertrophic cardiomyopathy have no symptoms and go about their daily lives normally, though they should avoid strenuous activities or competitive sports. Asymptomatic people should be screened for risk factors for sudden cardiac death. In patients with resting or inducible outflow obstructions, situations that produce dehydration or vasodilation (such as the use of vasodilatory or diuretic blood pressure medicines) should be avoided. People who are asymptomatic should forgo septal reduction therapy.
The main goal of medication is to relieve symptoms including chest pain, shortness of breath, and palpitations. Because beta blockers can lower heart rate and lessen the chance of ectopic beats, they are first-line drugs. Nondihydropyridine calcium channel blockers, such as verapamil, can be used in patients who can't take beta blockers, but they can be harmful if you have low blood pressure or severe shortness of breath at rest. These medications lower heart rates as well, although they should be used with caution in people who have significant outflow obstruction, high pulmonary artery wedge pressure, or low blood pressure. Dihydropyridine calcium channel blockers should be avoided in persons who have signs of blockage [1-5].
Author has no conflicts.