Prehospital Sudden Cardiac Death Research Articles

The epidemiological analysis of patients in pre-hospital sudden cardiac death for our large and medium sized cities

Objective To investigate the epidemiological information of patients in pre-hospital sudden cardiac death for our large and medium-sized cities and probe the patients' characteristic. Methods The death data in 2008 were exported from the computer databases of 8 large and medium-sized cities' emergency medical centers in our country. The thorough records of death data were conducted to statistical analysis. Results ①The scheduling time, running time, rescue time, returning time, total time and service radius in the sudden cardiac death group were (2. 12 ± 1.02 ), ( 14. 10 ± 7. 05 ), (24. 79 ± 12.08 ), ( 13.79 ± 6.61 ), (54. 80 ± 25. 36 ) minutes and 7.90 ± 3.92 (km)respectively. ②The patients' amount of sudden cardiac death group was at most in first quarter, and the most time slice of patients' amount was 8:00 ～ 10:00, and the least time slice of patients' amount was 2:00 ～ 4:00. ③The sudden cardiac death amount of male patients was more than that of female patients, and its age was less than that of female patients. ④The percentage of witness' CPR was 4.48%, and the success rates of medical care personnel' CPR was 2. 26%. Conclusion ①The sudden cardiac death is the overriding reason of death in our large and medium-sized cities. ②It is very important to cut the death rate of the middle-old age patients by strengthening prevention and cure of cardiovascular diseases, discerning the critical illness early,improving the level of pre-hospital medical care and popularizing CPR to public. Key words: Pre-hospital medical care; Sudden cardiac death; Epidemiological analysis

Birthplace in area with high coronary heart disease mortality predicts the severity of coronary atherosclerosis among middle-aged Finnish men who had migrated to capital area: The Helsinki Sudden Death Study

Background. Reasons why eastern-born male Finns have higher coronary heart disease (CHD) mortality than do western-born men are still unsettled. Recently, eastern birthplace was found to be an independent predictor of pre-hospital sudden cardiac death (SCD) in the new low-mortality area of residence.Aim. To investigate the association of birthplace with high CHD mortality attributes to more severe coronary atherosclerosis among men migrated to the low-mortality capital area.Method. Coronary atherosclerosis was measured in 373 western-born and 314 eastern-born out-of-hospital male deaths aged 33–70 years in Helsinki (The Helsinki Sudden Death Study), covering 24.6% of male deaths within this age-group. CHD risk factors were obtained from an interview of a next of kin.Results. In multivariate analysis there was a strong birthplace-by-age interaction with atherosclerosis (P = 0.0005). Eastern-born men <54 years had larger areas of fatty streaks (P = 0.0195), fibrotic plaque (P = 0.0133), calcification (P = 0.0009), total plaque area (P = 0.0011), and greater stenosis (P = 0.0004) in the left coronary compared to western-born men, independent of CHD risk factors. Amongst older men (≥54 years) such an association no longer appeared.Conclusion. Higher CHD mortality among eastern-born men may be due to more severe coronary atherosclerosis independently of CHD risk factors, reflecting Finns' two-phase settlement history.

Interleukin 18 gene promoter polymorphism: a link between hypertension and pre-hospital sudden cardiac death: the Helsinki Sudden Death Study

The interleukin 18 (IL-18) gene has a single nucleotide promoter region (-137) G-to-C polymorphism (rs187238) which leads to attenuated transcriptional activity of the gene and to lower production of pro-atherogenic IL-18. The C allele of this polymorphism is associated with a lower risk of sudden cardiac death (SCD). We examined the process by which this polymorphism alters the risk of SCD and coronary artery disease (CAD) by analysing the interactions between this polymorphism and environmental factors. TaqMan 5' nuclease assay was used to genotype the study population of the Helsinki Sudden Death Study, comprising medicolegal autopsies of 700 men. According to adjusted logistic regression analysis, there was a significant interaction between IL-18 genotype and hypertension impacting on the risk of SCD due to coronary heart disease (CHD) (P = 0.011) and the severity of autopsy-verified CAD (P = 0.026). Among GG homozygotes, hypertension was a major risk factor for SCD due to CHD [adjusted odds ratio (OR) 3.75 with 95% CI 1.78-7.91, P < 0.001] and hypertension also associated with larger coronary atherosclerotic plaque areas (P = 0.002) and the occurrence of complicated plaques (adjusted OR 8.38 with 95% CI 2.39-29.33, P < 0.001). Among C allele carriers, hypertension was not a significant risk factor for CHD-related SCD or CAD and did not associate with the development of coronary atherosclerotic plaques. According to gene expression analysis of atherosclerotic tissue samples obtained from live patients, hypertension also interacted significantly with IL-18 genotype affecting the expression of IL-18 (P = 0.030) mRNA and interferon-gamma mRNA (P = 0.004). Hypertension interacts with IL-18 gene promoter -137 G/C polymorphism, affecting the risk of SCD and the development of coronary atherosclerosis.

Birthplace predicts risk for prehospital sudden cardiac death in middle-aged men who migrated to metropolitan area: The Helsinki Sudden Death Study

Background. Eastern-born male Finns, irrespective of their place of residence, have high mortality from coronary heart disease (CHD), and half of such deaths are sudden.Aim. To study whether eastern birthplace alone or combined with life-style factors predicts risk for prehospital sudden cardiac death (SCD) in the new (west) low-mortality area of residence.Method. Prospective case-control autopsy study of all (700) out-of-hospital deaths of men aged 35–69 years in metropolitan Helsinki during 1981–82 and 1991–92. Data on CHD risk factors were obtained for 405, of whom 149 died of SCD (cases) and 256 of other causes (controls).Results. A birthplace-by-age interaction with SCD (P=0.024) and with myocardial infarction (P=0.005) appeared. Men ≤54 years born in the east were more often victims of SCD (odds ratio 2.99, 95% confidence interval 1.38–6.49, P=0.006) than were men born in the west, independently of CHD risk factors. SCD was predicted also by alcohol consumption, age, smoking, and hypertension. Amongst older (>54 years) men no association with birthplace was any longer evident, but alcohol and socio-economic status predicted SCD.Conclusions. Birthplace-based risk for SCD suggests the contribution of early life environment or genetic east-west differences, reflecting Finns’ two-phase settlement history.

Expression of sterol regulatory element-binding transcription factor (SREBF) 2 and SREBF cleavage-activating protein (SCAP) in human atheroma and the association of their allelic variants with sudden cardiac death

BackgroundDisturbed cellular cholesterol homeostasis may lead to accumulation of cholesterol in human atheroma plaques. Cellular cholesterol homeostasis is controlled by the sterol regulatory element-binding transcription factor 2 (SREBF-2) and the SREBF cleavage-activating protein (SCAP). We investigated whole genome expression in a series of human atherosclerotic samples from different vascular territories and studied whether the non-synonymous coding variants in the interacting domains of two genes, SREBF-2 1784G>C (rs2228314) and SCAP 2386A>G, are related to the progression of coronary atherosclerosis and the risk of pre-hospital sudden cardiac death (SCD).MethodsWhole genome expression profiling was completed in twenty vascular samples from carotid, aortic and femoral atherosclerotic plaques and six control samples from internal mammary arteries. Three hundred sudden pre-hospital deaths of middle-aged (33–69 years) Caucasian Finnish men were subjected to detailed autopsy in the Helsinki Sudden Death Study. Coronary narrowing and areas of coronary wall covered with fatty streaks or fibrotic, calcified or complicated lesions were measured and related to the SREBF-2 and SCAP genotypes.ResultsWhole genome expression profiling showed a significant (p = 0.02) down-regulation of SREBF-2 in atherosclerotic carotid plaques (types IV-V), but not in the aorta or femoral arteries (p = NS for both), as compared with the histologically confirmed non-atherosclerotic tissues. In logistic regression analysis, a significant interaction between the SREBF-2 1784G>C and the SCAP 2386A>G genotype was observed on the risk of SCD (p = 0.046). Men with the SREBF-2 C allele and the SCAP G allele had a significantly increased risk of SCD (OR 2.68, 95% CI 1.07–6.71), compared to SCAP AA homologous subjects carrying the SREBF-2 C allele. Furthermore, similar trends for having complicated lesions and for the occurrence of thrombosis were found, although the results were not statistically significant.ConclusionThe results suggest that the allelic variants (SREBF-2 1784G>C and SCAP 2386A>G) in the cholesterol homeostasis regulating SREBF-SCAP pathway may contribute to SCD in early middle-aged men.

Age-dependent association between hepatic lipase gene C-480T polymorphism and the risk of pre-hospital sudden cardiac death: The Helsinki Sudden Death Study

Objective We investigated the association between hepatic lipase (HL) C-480T polymorphism and the risk of acute myocardial infarction (AMI) as well as pre-hospital sudden cardiac death (SCD). Methods Seven hundred sudden or unnatural pre-hospital deaths of middle-aged (33–70 years, mean 53 years) Caucasian Finnish men were subjected to detailed autopsy (Helsinki Sudden Death Study). Genotype data were obtained for 682 men. Results In logistic regression analysis with age, body mass index, hypertension, diabetes, smoking and alcohol consumption as covariates, men with the TT genotype had an increased risk for SCD and AMI compared to CC carriers (OR = 3.0, P = 0.011; and OR = 3.7, P = 0.003). There was a significant age-by-genotype interaction ( P < 0.05) on the risk of SCD. Compared to CC genotype carriers, the association between the TT genotype and SCD was particularly strong ( P = 0.001) among men <53 years of age, but this association was non-significant among older men. This was mainly due to a strong association between the TT genotype and AMI due to severe coronary disease in the absence of thrombosis. Carriers of the TT genotype were more likely to have severe coronary stenoses (≥50%) than men with the CT or CC genotype ( P = 0.019). Conclusions The results suggest that HL C-480T polymorphism is a strong age-dependent risk factor of SCD in early middle-aged men.

Radiographic Assessment of Dental Health in Middle-aged Men Following Sudden Cardiac Death

Poor oral health has been suggested to be a risk factor for myocardial infarction. To study if dental pathology might predispose to pre-hospital sudden cardiac death, and using a sum index of panoramic tomography findings, we compared the oral health of middle-aged (33-69 yrs) male victims (Helsinki Sudden Death Study) of sudden cardiac death (n = 117) with that of controls, who died of non-cardiac diseases (n = 63) or suffered unnatural sudden death (n = 120). The mean number of teeth was 15.2, and 17.4% of the men were edentulous. Frequent age-associated findings in dentate victims were fillings (79.9%), horizontal bone loss (72.1%), periapical lesions (45.6%), residual roots (38.2%), and vertical pockets (30.9%). In multivariate analysis with coronary heart disease risk factors and number of teeth as covariates, poor oral health was associated (p = 0.053) with the risk of sudden cardiac death along with age, smoking, and body mass index. This association was especially strong (p = 0.009) among victims < 50 yrs.

Management of the patient who has been resuscitated from sudden cardiac death.

CD is a 68-year-old man who had an anterior myocardial infarction 6 months ago. Evaluation at that time demonstrated an occluded left anterior descending artery, which was successfully stented with no other significant lesions. Left ventricular ejection fraction was 35%. He had no recurrent angina or heart failure symptoms. Early one morning he lost consciousness. Paramedics verified ventricular fibrillation (VF) and provided effective defibrillation within 5 minutes; spontaneous circulation returned before transfer to the hospital. Sudden cardiac death claims 300 000 to 450 000 lives a year in the United States and represents approximately 50% of all cardiac death.1–3⇓⇓ Despite recent declines in age-adjusted cardiac mortality and sudden death risk, the overall incidence has remained relatively stable as our population ages.3 Coronary heart disease is present in the majority (70% to 80%) of patients with sudden death, but cardiac arrest is the first manifestation of this underlying process in 50%.4 Resuscitation rates are very low, averaging from 1% to 3% in most major cities.2,5⇓ There are some data to suggest that focused attempts to reduce the time to effective defibrillation, with improved training of first responders or more widespread availability of automatic external defibrillators, provide some hope for the future. It is a widely held belief that the majority of sudden death events are due to ventricular tachycardia (VT) that degenerates into VF (Figure 1).6 This idea may well reflect our greater experience in observing patients with structural heart disease and prior myocardial infarction. Acute severe ischemia may cause primary polymorphic VT even in the absence of preexisting structural heart disease. Autopsy studies document acute changes in coronary morphology (such as plaque rupture, thrombus, etc) in >50% of sudden death events.7 Severe bradyarrhythmias or electromechanical dissociation probably represent an important …

Comparison of Prehospital Monomorphic and Polymorphic Ventricular Tachycardia: Prevalence, Response to Therapy, and Outcome

Objective: Monomorphic ventricular tachycardia (MVT) is the most common form of prehospital ventricular tachycardia (VT). Recent literature suggests that polymorphic ventricular tachycardia(PVT) is more common during cardiopulmonary arrest than previously thought but responds poorly to advanced cardiac life support (ACLS) therapy. We undertook this study to determine the prevalence, response to therapy, and outcome of both MVT and PVT in the prehospital sudden cardiac death victim. Design: Retrospective prehospital chart review from 1987 to 1991. Setting: Municipal, fire departmentbased, multitiered emergency medical system serving a population of approximately one million. Participants: Adult patients older than 18 years experiencing prehospital, nontraumatic cardiopulmonary arrest with VT occurring at any time during the resuscitation. VT was defined as PVT if the QRS-complex configuration was not stable when viewed in a single electrocardiographic lead (ie, episodic changing of the QRS-complex electrical axis, amplitude, or both or the presence of more than two QRS-complex morphologies). Outcome was defined in terms of both the presence or absence of spontaneous circulation at the end of the prehospital phase of care and ultimate outcome (survival to hospital discharge or death). Four hundred seventy-six patients met entry criteria; 37 patients were excluded because of incomplete medical records, and 439 patients were used for data analysis. Interventions: ACLS therapy based on the 1987 American Heart Association guidelines. Results: MVT occurred in 323 patients (73.6%), with 119 (36.8%) showing return of spontaneous circulation (ROSC) in the prehospital setting; 35 MVT patients(10.8%) survived to hospital discharge. PVT occurred in 116 patients (26.4%), with 48 (41.4%) showing ROSC in the prehospital setting; 15 PVT patients (12.9%) survived to hospital discharge. The use of ACLS therapy (defibrillation, endotracheal intubation, medication usage) between the two rhythm groups was not statistically different. The P values for ROSC, ultimate outcome, and use of ACLS therapy were all not significant. Conclusion: We conclude that PVT is a common rhythm occurring in prehospital cardiopulmonary arrest that responds as well as MVT to ACLS therapy. Until prospective data are available, standard ACLS therapy should be used in all forms of prehospital VT occurring during cardiopulmonary arrest. [Brady W, Meldon S, DeBehnke D: Comparison of prehospital monomorphic and polymorphic ventricular tachycardia: Prevalence,response to therapy, and outcome. Ann Emerg Med January 1995;25:64-70.]

Long-term follow-up of survivors of prehospital sudden cardiac death treated with coronary bypass surgery

Although coronary artery bypass surgery is beneficial to patients with severe coronary artery disease, its role in preventing the recurrence of prehospital cardiac arrest in patients is not clear. In this article, we report on the long-term follow-up of 49 survivors of prehospital coronary arrest who had coronary artery bypass surgery. Prior to their prehospital cardiac arrest, 14% of the patients had a history of unstable angina. Coronary angiograms obtained after prehospital cardiac arrest showed that 71% of the patients had three-vessel coronary artery disease and 6% had single-vessel disease. The mean left ventricular ejection fraction was 45%. There were four postoperative deaths; three were caused by pump failure, and one was caused by refractory ventricular arrhythmias. After a maximum follow-up period of 102 months (mean of 55.4 months), there were seven cardiac deaths; five of the patients died of recurrent ventricular fibrillation, and two patients; deaths were related to refractory heart failure. Actuarial analyses of the 49 patients showed that the probability of survival at 6 months, 1 year, 2 years, 3 years, and 5 years was 92%, 92%, 89%, 82%, and 72%, respectively. After surgery, 35 of the 45 patients who were discharged from the hospital were asymptomatic, and 23 of the 32 patients who were employed when their prehospital cardiac arrest occurred returned to their employment. We concluded that coronary artery by pass surgery is beneficial to certain survivors of prehospital sudden death. After surgery, most patients are asymptomatic and capable of returning to their employment and the recurrence of prehospital sudden death is low.

Long-term survival after prehospital sudden cardiac death

One hundred thiry-nine survivors of prehospital sudden cardiac death were followed after their hospital discharge. Eighty patients were studied with coronary angiography and cardiac catheterization; 34 of these underwent coronary bypass surgery. After a maximum follow-up of 105 months, 89 patients were still alive. The probability of survival at 6 months, 1 year, 2 years, 3 years, 4 years, and 5 years was 88%, 86%, 78%, 70%, 63%, and 59%, respectively. Of the 43 cardiac deaths, 37 (86%) were secondary to documented recurrent ventricular fibrillation or occurred suddenly. Twelve percent of the total population had recurrent ventricular fibrillation in the first year following the initial cardiac arrest, 16% within 2 years, and 22% within 3 years. Of the 37 survivors dying from recurrent ventricular fibrillation, 32% died within the first 3 months following hospital discharge, 46% in the first year, 64% within 2 years, and 78% within the first 3 years. Most survivors were capable of resuming normal activities after hospital discharge. Only 7% demonstrated permanent neurologic impairment. Sixty-eight percent of the patients who were employed at the time of their prehospital sudden cardiac arrest returned to full-time employment. In the subset of 34 surgically treated patients, there have been six (18%) cardiac deaths. Four of these deaths were related to recurrent ventricular fibrillation, with one of these deaths occurring in the immediate postoperative period. The other three deaths related to recurrent ventricular fibrillation occurred 36 months (two deaths) and 49 months following the initial prehospital cardiac arrest.

Pathophysiologic observations in prehospital ventricular fibrillation and sudden cardiac death.

In order to better understand the problem of prehospital sudden cardiac death (SCD) two groups of individuals were studied. One group was monitored by rescue squads during attempted rescue. These subjects were defibrillated from prehospital ventricular fibrillation (VF) and hospitalized if they survived or autopsied if they could not be resuscitated. The second group were SCDs which were witnessed and described by observers. Detailed past histories of both groups were collected, and either clinical or autopsy diagnoses were obtained. On the day of death or VF, one quarter reported new symptoms (primarily chest pain and dyspnea) preceding collapse by more than 30 minutes, one quarter reported symptoms lasting from 1 to 30 minutes, and one half collapsed instantaneously or within 1 minute of acute symptoms. A history of old myocardial infarction (MI) was present in 41% and of angina pectoris in 54%, and 27% reported new or changing symptoms within four weeks. In defibrillated survivors, "would-be SCDs," electrocardiographic (ECG) changes of acute myocardial infarction (AMI) or ischemia were nearly three times more frequent than changes detected histologically in SCDs, and in the former involved predominantly the anterior wall in contrast to the inferior wall in most autopsied deaths. This disparity implicates acute myocardial lesions, particularly of the anterior wall, in the majority of SCDs. Acute coronary lesions were found in 58% of SCDs autopsied. Most of these were ruptured plaques although almost one fifth of all autopsied SCDs had thromboses without intimal rupture. Severe chronic multivessel stenosis was present in most subjects, although 15% had only disease of a single vessel and in these, the left anterior descending (LAD) or left main coronary artery were involved in three quarters. The SCD population may be subgrouped into those with recent MI, those with only myocardial ischemia, and those with no detectable myocardial change. When rescuers were able to monitor prehospital SCDs, VF was found in the majority; however, 28% did have other terminal rhythms.