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Transcript
What physical activities that are safe for high risk patient? Farial Indra Regular physical activity offers a variety of health benefits not only in the general, healthy population, but also in subjects with cardiac diseases. Prevention of coronary artery disease, Prevention of stroke, Prevention of cancers, Reduction of mortality, Other beneficial effects of exercise include modification of cardiovascular risk profiles, such as control of hypertension, improved lipid profile, prevention of type 2 diabetes, benefit on the bone-mineral metabolism and body composition. A significant relationship between physical activity and reduction in mortality has been reported, with a mortality reduction reaching up to 20-40%. A clear dose-response relationship was established and a larger volume of physical activity was related with a lower all-cause mortality. This inverse dose-response relationship has been shown both in men and women, in younger and older subjects.The updated recommendation specified that “All healthy adults aged 18-65 need moderate-intensity aerobic physical activity for a minimum of 30 minutes on five days each week or vigorous-intensity aerobic activity for a minimum of 20 minutes on three days each week”. To meet the current recommendation, the minimum expenditure should be in the range of 450-750 MET×minutes per week. Vigorous physical activity can precipitate acute myocardial infarction (AMI) or sudden cardiac death. A prospective study from the Veneto Region of Italy states that adolescents and young adults (<35 y.o.) engaged in competitive sports have an increased risk of SCD, compared with their non-athletic counterparts (the annual incidence of SCD was 2.3 in 100,000 in competitive athletes compared with 0.9 in nonathletes, with an estimated relative risk of 2.5). About 90% of all SCD were exerciserelated in athletes, while only 9% of all SCD were related with exercise in the nonathletes group. It is generally accepted that sports, per se, is not a cause of increased mortality; rather, it acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to life-threatening ventricular arrhythmias. sudden cardiac death risk prediction The risk of SCD increases with advancing age, peaking in the 75–84 year age group. most SCD cases (≥80%) have associated coronary artery disease (CAD). Other associated conditions include dilated or hypertrophic cardiomyopathy (10–15% cases) and a smaller subgroup (5–10%) have primary genetic or congenital disorders, such as long QT syndrome, Brugada syndrome, congenital structural heart disease or sudden unexplained death (sudden death with structurally normal heart but no identifiable genetic etiology), CAD that constitute the vast majority, there are no established risk factors that can be used to identify a high-risk patient. At present, severe left ventricular (LV) systolic dysfunction, who have an LVEF <30–35% are considered to be high-risk. Relatively rare primary genetic syndromes such as long QT syndrome and hypertrophic cardiomyopathy patients qualify as high-risk based on a combination of familial and individual clinical history, as well as the identification of specific genetic mutations that are associated with higher risk. Mechanism of sudden cardiac death or ventricular fibrillation In acute ischemia and sympathetic activation, lead to a markedly increased dispersion of repolarization and cell-to-cell conduction, which ultimately leads to ventricular fibrillation (VF). In heart failure, sympathetic stimulation,lead to spontaneous Ca++ release and enhanced Na-Ca exchange, together with IK1 reduction, results in greater propensity for developing delayed after-depolarization. In Hypertrophic cardiomyopathy, heterogeneous substrate may be prone to develop ventricular tachyarrhythmias during exercise, due to outflow tract obstruction, myocardial ischemia or sympathetic surge. In Arrhythmogenic right ventricular dysplasia, SCD is frequently the first manifestation of the disease, and it occurs relatively frequently during exercise or stress. RV dilation, precordial repolarization abnormalities, and LV involvement have been associated with higher risk of sudden death. In Coronary artery anomaly, Cardiac events occur mainly during intense exertion probably provoked by myocardial ischemia from angulation of the coronary ostium or compression of the coronary artery. Premonitory symptoms (syncope, chest pain) may occur shortly before the onset of sudden death. In The Wolff-Parkinson-White syndrome, the main mechanism of SCD seems to be atrial fibrillation conducting rapidly over an accessory pathway and degenerating into VF. In Long QT syndrome Arrhythmic events are often associated with physical exercise, emotional stress or auditory stimulation in long QT type 1 or 2. Swimming is a relatively genotype-specific arrhythmogenic trigger for type 1 of the long QT syndrome and catecholaminergic polymorphic ventricular tachycardia (CPVT). type 2 LQTS patients are susceptible to auditory stimulation or alarm.. in patients with short QT syndrome, Cardiac events may occur during effort or loud noise, but this association weaker than in both LQTS and CPVT. Exercise recommendations Individual clinical judgment is required for patients with high risk clinical features, such as history of important cardiac symptoms, including syncope, prior cardiac operation, heart transplantation, presence of an implanted cardioverter-defibrillator or pacemaker, potentially life-threatening arrhythmias or other evidence of high-risk status. Exercise training in patients with HF is safe and has numerous benefits. Meta-analyses show that cardiac rehabilitation reduces mortality; improves functional capacity, exercise duration, and Health-Related Quality of Life (HRQOL); and reduces hospitalizations. Patients with genetic cardiovascular diseases (GCVDs) are at higher risk for SCD during exercise compared with normal subjects. Exercise under extreme adverse environmental conditions, intense static exertion (weight lifting), Activities requiring sudden acceleration or deceleration (burst exertion), exercises with potential risk of traumatic injury associated with loss of consciousness (free-weight lifting, rock climbing or ice hockey) or with possibilities of impaired consciousness during water-related activities are generally either not advised or strongly discouraged in all forms of genetic cardiovascular diseases. the known benefits and potential adverse outcomes of exercise requires careful weighing of the perceived risk to benefit ratio for each patient. Patients with GCVDs can safely participate in most forms of recreational exercise of moderate or low intensity (i.e., equivalent to or lower than 6 METs). A moderate intensity physical activity program has low rate of cardiovascular complications in asymptomatic persons. proper exercise is defined as several months of mild-to-moderate physical activity or intensity-controlled-exercise training consisting of walking, jogging, swimming, skiing, or cycling 3 to 4 times a week. For every additional time per week an individual was habitually exposed to physical activity, the RR for MI decreased by approximately 45%, and the RR for SCD decreased by 30%. Acute cardiac events were significantly associated with episodic physical and sexual activity; this association was attenuated among persons with high levels of habitual physical activity. The intensity of exercise is expressed as percent of VO2 max or percent of maximal heart rate (HR). Moderate intensity exercise is that performed at a relative intensity of 40% to 60% of VO2 max, For moderate-intensity exercise, a person’s target heart rate should be 50 to 70% of his or her maximum HR. This estimate of maximum HR is based on the person’s age. It can be obtained by subtracting the person’s age from 220. Thus, the formula of the HR of moderate-intensity exercise is : HR= (50% to 70%)*(220-age).