SUDDEN CARDIAC DEATH/ARREST Sudden cardiac death ( SCD/SCA) is an unexpected death due to cardiac causes that occurs in a short time period (generally within 1 hour of symptom onset) in a person with known/unknown cardiac disease Patients at risk for SCD may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints.
THE CHRONOLOGY …
SCA is not a random event. Most victims do have heart disease or other health problems, often without being aware of it . As many as 75 % of people who die of SCA show signs of a previous heart attack . Eighty percent have signs of coronary artery disease Approximately 92% of those who experience SCA do not survive. SCA kills more than 1,000 people a day, or one person every 90 seconds
EPIDEMIOLOGY Nearly two thirds of cardiac arrests occur as the first clinically manifested event or in the clinical setting of known disease in the absence of strong risk predictors. Less than 25% of the victims have high-risk markers based on arrhythmic or hemodynamic parameters General patterns of heightened risk during the morning hours, on Mondays, and during the winter months have been described .
The incidence of SCD increases markedly with age regardless of sex or race but the proportion of deaths that are sudden is larger in the younger age groups CHD is the most common substrate underlying SCD After a MI the most rapid rate of attrition occurs during the first 6 to 18 months after the index event . A secondary delayed increase in risk occurs in post–myocardial infarction patients 2 to 5 years after an index event, probably related to ventricular remodeling and heart failure .
SCA – INDIAN PERSPECTIVE Annual incidence of SCA in India is 0.55 per 1000 population SCA accounts for >50% of cardiovascular deaths in India The peak age of SCA occurrence is between 45 and 75 years, with a higher preponderance in men (3:1) Survival rate of SCA is <1 % Fortis Hospital , New D elhi - statistics
SOUTH INDIAN STUDY The proportion of SCD among total mortality in a population in Southern India using a questionnaire-based approach was assessed RESULTS : Out of 2185 deaths, 1691 (77.4%) were recallable . A total of 173 (10.3%; 128 M and 45 F; mean age - 60.8 ± 14 years) deaths were adjudicated as SCD. Of these, 82 (47.3%) were ≤ 60 years of age. Prior MI, LV dysfunction and prior aborted SCD were found in 33.5%, 22.5% and 5.7% respectively.
CAD was observed in 66 (38%) and AMI in 30 (17%). At least 1 of 3 CAD risk factors - hypertension, diabetes, or smoking was observed in 80.6%. Proportion of subjects with at least one risk factor for CAD were similar in the age groups above and below 50 years (67.6% vs. 81.7%, p=0.065 ). CONCLUSIONS : SCD contributed to 10.3% of overall mortality On an average, SCD cases were 5-8 years younger compared to populations reported in the western hemisphere Rao BH et al , Contribution of sudden cardiac death to total mortality in India - a population based study ; Int J Cardiol . 2012 Jan 26;154(2): 163-7
RISK FACTORS OF SCD GENETIC FACTORS CHD RISK FACTORS ARRHYTHMIAS NUTRITIONAL PSYCHOSOCIAL FACTORS BIOMARKERS – AS RISK FACTORS
GENETIC CONTRIBUTORS TO SCD RISK Genetically Based Primary Arrhythmia Disorders Congenital long-QT interval syndrome, short-QT syndrome Brugada syndrome Catecholaminergic polymorphic (“idiopathic”) VT/VF Inherited Structural Disorders with Arrhythmic SCD Risk Hypertrophic cardiomyopathy Right ventricular dysplasia/cardiomyopathy Genetic Predisposition to Induced Arrhythmias and SCD Drug-induced “acquired” LQTS (drugs , electrolytes ) Electrolyte and metabolic arrhythmogenic effects
RISK FACTORS COMMON TO BOTH CHD & SCD NON MODIFIABLE Age Male Gender F/H/O CHD Genetic Factors MODIFIABLE Smoking Hypertension H yperlipidemia Diabetes Mellitus Obesity Renal dysfunction Sedentary lifestyle
CORONARY ARTERY DISEASE In the Framingham Study , preexisting CAD was associated with a 2.8- to 5.3-fold increase in risk of SCD Both left ventricular dysfunction and NYHA class were powerful risk factors for SCD in patients with either ischemic or nonischemic cardiomyopathy An LVEF of less than 30 % (due to any etiology ) is the single most powerful independent indicator for SCD
ARRHYTHMIAS PVCs and nonsustained VT during both the exercise and recovery phases of a stress test are predictive of increased risk Arrhythmias in the recovery phase appear to predict a higher risk than arrhythmias in the recovery phase A frequency cutoff of 10 PVCs/hour as a threshold level for increased risk is cited by most studies
ECG MARKERS Elevated resting heart rate Prolonged QRS duration Abnormal heart rate recovery (HRR < 12 bpm 1st min , < 22bpm after 2 min) Prolonged QT interval and Early repolarization syndrome ( horizontal or descending ST segments in inferior / lateral leads)
NUTRITIONAL RISK FACTORS Increased consumption of n-3 polyunsaturated fatty acids is inversely associated with SCD to a greater extent than nonfatal MI Heavy alcohol consumption ( > 5 drinks per day) is associated with an increased risk of SCD In contrast, light-to-moderate levels of alcohol consumption ( < 0.5 to 1 drinks per day) may be associated with reduced risks of SCD . High magnesium diet – low risk of SCD
PSYCHOSOCIAL Lower socioeconomic status Depression Anxiety S ocial isolation and P sychological stress have all been linked to an increase in cardiovascular mortality in diverse populations
BIOMARKERS AS RISK FACTORS INFLAMMATORY MARKERS CRP IL-1 receptor Fibrinogen IL-6 METABOLIC MARKERS Aldosterone Cystatin C Renin Vitamin D and PTH NEUROHORMONAL MARKERS BNP / NT-pro-BNP
CAUSES CAUSES OF AND CONTRIBUTING FACTORS OF SCD Coronary artery abnormalities Hypertrophy of ventricular myocardium Myocardial diseases and heart failure Inflammatory, infiltrative, neoplastic, and degenerative processes Diseases of the cardiac valves Congenital heart disease Electrophysiologic abnormalities Electrical instability related to neurohumoral and CNS influences Sudden infant death syndrome and sudden death in children Miscellaneous causes
PATHOPHYSIOLOGY The most common electrophysiologic mechanisms leading to SCD are tachyarrhythmias such as ventricular fibrillation (VF) or ventricular tachycardia (VT). R eentry is the most important known mechanism of VT and VF at tissue level At the cellular level increased excitation or decreased repolarization reserve of cardiomyocytes may result in ectopic activity ( eg automaticity, triggered activity), contributing to VT and VF initiation.
At the subcellular level, altered intracellular Ca2+ currents, altered intracellular K+ currents (especially in ischemia), or mutations resulting in dysfunction of a sodium channel can increase the likelihood of VT and VF . Approximately 20-30% of patients with documented sudden death events have bradyarrhythmia or asystole at the time of initial contact Sometimes an asystole and pulseless electrical activity (PEA) may result from a sustained VT
Most cases of SCD occur in patients with structural abnormalities of the heart Patients who survive a myocardial infarction, the presence of PVCs, particularly complex forms such as multiform PVCs, short coupling intervals (R-on-T phenomenon), or VT (salvos of 3 or more ectopic beats), reflect an increased risk of sudden death
CLINICAL FEATURES Patients at risk for SCD may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints. History and associated symptoms, to some degree depend on the underlying etiology of SCD A prior history of LV impairment (ejection fraction < 30-35%) is the most potent common risk factor for sudden death.
Coronary artery disease Previous cardiac arrest Syncope Prior myocardial infarction, esp within 6 months Ejection fraction less than 30-35% H/O frequent ventricular ectopy ( > 10 PVC/h or NSVT) Dilated cardiomyopathy Previous cardiac arrest Syncope Ejection fraction less than 30-35% Use of inotropic medications
3. Hypertrophic cardiomyopathy Previous cardiac arrest Unexplained Syncope ( recent , in young) Family history of one or more premature HCM-related deaths, particularly if sudden and multiple Symptoms of heart failure Drop in SBP or ventricular ectopy upon stress testing Palpitations M ultiple , repetitive (or prolonged) nonsustained bursts of ventricular tachycardia on serial ambulatory ( Holter ) ECGs M assive LV hypertrophy (wall thickness, ≥30 mm), particularly in young patients
4. Valvular disease Valve replacement within 6 months Syncope History of frequent ventricular ectopy Symptoms associated with severe uncorrected AS/MS 5. Long QT syndrome Family history of long QT and SCD Medications that prolong the QT interval Bilateral deafness
Thompson and McCullough Cardiac A rrest S core ED SBP greater than 90 mm Hg = 1 point ED SBP less than 90 mm Hg = 0 points Time to ROSC less than 25 minutes = 1 point Time to ROSC more than 25 minutes = 0 points Neurologically responsive = 1 point Comatose = 0 point Maximum score = 3 points Patients with a score of 3 points can be expected to have an 89% chance of neurologic recovery and an 82% chance of survival to discharge
INVESTIGATIONS Cardiac enzymes Electrolytes Drug Toxicology screen BNP
IMAGING ECG Signal averaged ECG (micro T wave alternans – high NPV) 2D ECHO Nuclear imaging techniques Coronary angiography Electrophysiological studies