“Hypertrophic cardiomyopathy (HCM) is the most common cause of SCD in athletes younger than 35 years of age.”
The lethal cardiovascular disease that is now omnipresent in young athletes poses a complex dilemma regarding sportsperson safety, patient autonomy, team or institutional risk tolerance and medical decision-making. The goodness of regular exercise on cardiovascular health and all‐cause mortality are well established. However, the recent studies have demonstrated that nearly threefold increased risk of sudden cardiac death (SCD) is found in young athletes with underlying cardiovascular conditions when compared to sedentary individuals. Hypertrophic cardiomyopathy (HCM) is the most common cause of SCD in athletes younger than 35 years of age.
“The people associated with any sports usually perform intensive and regular exercise to maintain their fitness and they thereby develop a variety of electrical and structural cardiac adaptations.”
The people associated with any sports usually perform intensive and regular exercise to maintain their fitness and they thereby develop a variety of electrical and structural cardiac adaptations that eventually manifest them to improve the stroke volume, reflexes that invariably enhance their performance. Greater left ventricular (LV) wall thickness is seen more compared to sedentary controls in nearly one-fifth of young athletes (aged between 14–35 years).
The usual cause for tiredness are iron deficiency, viral infections, asthma-like conditions, medication, mood disturbance and endocrine conditions such as PCOS or RED-S and the non-medical causes causes of tiredness in the athlete are an inappropriate training plan, poor sleep, lifestyle stressors, inadequate macronutrient intake and suboptimal hydration. Apart from this, nutrition plays an important part in the life of a sportsperson. As these patients are considered to be at high risk of sudden cardiac death (SCD) during exercise hence it is kind of reserved for them and hence sedentary lifestyle is advisable to them.
In India the need for contemporary public and physician awareness towards the broad spectrum of HCM should be developed through the training and educational mode. The healthcare system should be upgraded and an expert technical team pertaining to developing advanced HCM-specific cardiac imaging, interpretative echocardiography and cardiovascular magnetic resonance need to be made. Another important initiatives involve access to adequate numbers of trained medical and paramedical personnel to support expanding defibrillator implant programmes, as well as the identification of surgeons experienced in septal myectomy. With the increase in impact of advanced heart failure and the option of transplant now we have greater relevance to the multidisciplinary approach for HCM.
In terms of priority the standard imagining and clinical evaluation has more importance than laboratory-based genetic testing for HCM management. Proposed hierarchical model as an approach to developing dedicated hypertrophic cardiomyopathy (HCM) programmes, with components and treatment options arranged with respect to initial priority. AF, atrial fibrillation; ASA, alcohol septal ablation; CMR, cardiovascular magnetic resonance; ICD, implantable cardioverter defibrillator; SD, sudden death.
“The latest data showed a steep increase in the number of deaths of sportspeople and in certain cases they are restricted to sedentary lifestyles.”
Though slowly but steadily the HCM is causing a lot of havoc in the present healthcare system. The latest data showed a steep increase in the number of deaths of sportspeople and in certain cases they are restricted to sedentary lifestyles.
According to new research from the University of British Columbia, Canada gives us the study that even the fittest among the sportsperson are not immune to cardiovascular disease — and they often don’t have any symptoms. Another study published recently in the British medical journal Open Sport and Exercise Medicine highlights the importance for middle-aged athletes to have their doctor check their cardiovascular risk factors, when high blood pressure, high cholesterol, or diabetes are prevalent in their family history of cardiovascular disease. The inherited condition of familial hypercholesterolemia is a condition that is characterised by very high levels of cholesterol present in the blood.
“The inherited condition of familial hypercholesterolemia is a condition that is characterised by very high levels of cholesterol present in the blood.”
Cholesterol, a waxy, fat-like substance created within the body and obtained from foods that return from animals (particularly egg yolks, meat, poultry, fish and farm products), is needed by the body to form cell membranes, bound hormones and compounds that aid in fat digestion. In individuals with monogenic disorder, the body is unable to induce additional sterol, and it builds up within the blood. The surplus sterol is deposited on the inner walls of blood vessels, notably the arteries that offer blood to the guts (coronary arteries), forming clumps (plaques) that slender and harden artery walls. because the plaques get larger, they will clog the arteries and prohibit flow of blood to the guts. The build-up of plaques in coronary arteries causes a style of pain referred to as angina and greatly will increase a person’s risk of getting a coronary failure.
Familial hypercholesterolemia is sometimes caused by mutations in 3 genes — LDLR, APOB, or PCSK9. Changes within the LDLR sequence is the measure for the foremost common reason behind this condition. The LDLR sequence provides directions for creating a macromolecule known as LDL receptor. This kind of receptor binds to particles known as low-density lipoproteins (LDLs, legendary ordinarily as unhealthy cholesterol), that square measure the first carriers of sterol within the blood. By removing LDLs from the blood, these receptors play an essential role in controlling sterol levels. Some LDLR sequence mutations scale back the quantity of LDL receptors made inside cells.
Less ordinarily, hypercholesterolemia is caused by mutations within the APOB or PCSK9 sequence. Proteins made from these genes square measure essential for the traditional performance of LDL receptors. Mutations in any of those genes forestall cells from creating useful receptors or alter the receptors performance. Hypercholesterolemia results once beta-lipoprotein receptors falters to measure and are unable to get rid of sterol from the blood effectively. High LDLs within the blood creates risk of heart diseases at a younger age. As of now, only statins are given to control the situation and if genetic default is there then only the beta-blocker injections are of temporary remedy. There are presently no medical interventions that alter the natural course of HCM, however, myosin inhibitors have shown potential promise. Gene-silencing with CRISPR/Cas9 gene-editing technology might sometimes play a job within the hindrance of malady development before the intervention of clinical manifestations. Till then the shared deciding in areas of exercise prescription, play a pivotal measure and therefore are essential to boost the standard of life and survival of patients with HCM.
“Dr. Debleena Bhattacharya is the Associate Editor of InnoHEALTH magazine and working as an Assistant Professor in Marwadi University, Gujarat. Her area of interest lies in Environmental Biotechnology focusing on wastewater treatment.”
