Pathophysiologic Observations in Prehospital Ventricular Fibrillation and Sudden Cardiac Death

Liberthson, Richard R.; Nagel, Eugene L.; Hirschman, Jim C.; Nussenfeld, Sidney R.; Blackbourne, Brian D.; Davis, Joseph H.

doi:10.1161/01.cir.49.5.790

Cited by 306 publications

(52 citation statements)

References 60 publications

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“…1 In our study, the left ventricular ejection fraction was less than 0.40 in 82% of patients with VT and 79% of those with sudden death and failed to discriminate between the two groups, supporting the hypothesis that a lower ejection fraction indicates a larger infarct with a higher probability that an arrhythmogenic area is present.…”

Section: Resultssupporting

confidence: 81%

Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.

Stevenson¹,

Brugada²,

Waldecker³

et al. 1985

Circulation

100

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After the acute phase of myocardial infarction, patients who develop sustained ventricular arrhythmias present with either sudden death or ventricular tachycardia (VT). Although current evidence suggests that VT frequently precedes ventricular fibrillation (VF) in patients presenting with sudden death, the factors resulting in rapid deterioration of VT to VF have not been delineated in humans. To determine whether left ventricular function, coronary anatomy, or electrophysiologic characteristics could differentiate patients with sudden death from those with VT without sudden death, we compared results of cardiac angiography and programmed electrical stimulation in 42 patients referred for evaluation of sustained VT or surviving "aborted" sudden death for more than 9 days after myocardial infarction. By univariate analysis there were no differences between patients with sudden death and those with VT in age, time from myocardial infarction to VT or sudden death, ejection fraction (0.31 0.12 vs 0.29 + 0.09), or the number of patients with a major area of contracting myocardium supplied by an artery with a 50% or greater or a 70% or greater stenosis (84% vs 64% and 68% vs 41 %). Thirty-six percent of patients with sudden death but no patient with VT had two separate areas of infarction. During programmed electrical stimulation, a sustained ventricular arrhythmia was initiated in 100% of patients with VT and 73% of patients with sudden death and rapidly produced syncope in 67% of patients with sudden death but in only 5% of those with VT. This difference was due to the more frequent initiation of rapid polymorphic VT or VF (27% of patients) and to the shorter VT cycle length (242 + 31 vs 319 ± 69 msec) when monomorphic VT was induced in the group with sudden death. No difference was found in the number of extrastimuli required for initiation of a sustained ventricular arrhythmia. We conclude that (1) resting ventricular function and the potential for ischemia remote from the infarct fail to distinguish patients with sudden death from those with VT without sudden death, (2) electrophysiologic properties determining VT rate and stability are major determinants of the clinical presentation of VT after myocardial infarction, and (3) two separate areas of infarction may predispose to sudden death.

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Section: Resultssupporting

confidence: 81%

Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.

Stevenson¹,

Brugada²,

Waldecker³

et al. 1985

Circulation

100

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“…Numerous studies of cardiac arrest victims and survivors of aborted cardiac arrests have identified several potential causes of cardiac arrest, the most common of which is ventricular tachycardia (VT) or fibrillation (VF) due to either acute ischemia or reentry in a healed myocardial scar. [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] These studies have focused primarily on the patient with coronary artery disease, including patients with and without heart failure, and may not accurately indicate the frequency of various causes of death in the heart failure population. Heart failure is associated with activation of the sympathetic nervous system and electrolyte abnormalities that could affect arrhythmogenesis.122,24 In addition, heart failure patients are predisposed to systemic and venous thromboemboli that could precipitate cardiac arrest.…”

mentioning

confidence: 99%

Diverse mechanisms of unexpected cardiac arrest in advanced heart failure.

Luu¹,

Stevenson²,

Stevenson³

et al. 1989

Circulation

483

154

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To define the mechanisms of unexpected cardiac arrest in advanced heart failure, we reviewed the causes of cardiac arrest as established from electrocardiographic monitoring and from clinical and autopsy data in patients hospitalized for cardiac transplantation evaluation and management of advanced heart failure (mean left ventricular ejection fraction, 0.18 +/- 0.08) who were stable while on vasodilator and diuretic therapy such that hospital discharge to home was anticipated. Twenty-one cardiac arrests occurred in 20 of 216 (9%) such patients during a 4-year period. Heart failure was due to coronary artery disease with prior myocardial infarction in 13 patients and nonischemic cardiomyopathy in seven patients. The rhythm at the time of arrest was severe bradycardia or electromechanical dissociation (BA/EMD) in 13 (62%) patients. The precipitating cause of the BA/EMD arrest was coronary artery thrombosis or embolism in two patients, pulmonary embolism in one patient, hyperkalemia in two patients, and unexplained hypoglycemia in one patient. In seven of 13 (54%) patients, a precipitating cause of the bradycardia arrest could not be established. Only eight of 21 (38%) arrests were due to ventricular tachycardia or fibrillation (VT/VF), and all occurred in patients with prior myocardial infarction (p = 0.02 vs. BA/EMD arrests). Two VT/VF arrests were due to acute or recent infarction, and one patient had hyperkalemia. The patients who suffered a BA/EMD arrest were similar to those who had a VT/VF arrest in age, ventricular arrhythmia history, ventricular function, and serum potassium levels. Serum sodium levels were lower in patients with BA/EMD arrests (129 +/- 3 vs. 133 +/- 4 meq/l, p = 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Autopsy studies among the general population have consistently reported both severe and diffuse coronary artery stenosis among SCD victims. In fact, several studies have reported that >95% of SCD victims had at least 1 coronary artery with ≥75% stenosis, and the majority of victims had multivessel disease, with the prevalence of 3‐ or 4‐vessel disease as high as 60% 19, 24, 25, 26, 27. The lower prevalence of severe stenosis in the current study compared with the aforementioned studies may suggest that the multiple stressors associated with firefighting can trigger a sudden cardiac event in individuals with a lower overall burden of disease.…”

Section: Discussionmentioning

confidence: 99%

Pathoanatomic Findings Associated With Duty‐Related Cardiac Death in US Firefighters: A Case–Control Study

Smith

Haller

Korre

et al. 2018

JAHA

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BackgroundSudden cardiac death accounts for the greatest proportion of duty‐related deaths among US firefighters. Increased understanding of the pathoanatomic causes of sudden cardiac death and the risk associated with underlying cardiac pathologies is needed to develop evidence‐based screening recommendations.Methods and ResultsUsing autopsy data for duty‐related firefighter fatalities occurring between 1999 and 2014, this retrospective case–control study compared cardiac findings of male firefighters aged 18 to 65 years who died on duty of cardiac‐related causes with those who died of noncardiac trauma‐related causes. Data from 276 cardiac cases and 351 noncardiac trauma controls were analyzed. Among cardiac cases, the most prevalent (82%) underlying pathoanatomic substrate was comorbid coronary heart disease and cardiomegaly/left ventricular hypertrophy. Cardiac cases had a higher prevalence of cardiomegaly (heart weight >450 g), left ventricular hypertrophy (left ventricular wall thickness ≥1.2 cm), and severe coronary artery stenosis (≥75%) than trauma controls (all P<0.001). In multivariate analyses, heart weight >450 g, coronary artery stenosis ≥75%, and evidence of a prior myocardial infarction were strong independent predictors of cardiac death, with odds ratios of 6.1 (95% confidence interval, 3.6–10.4), 9.3 (95% confidence interval, 5.3–16.1), and 6.2 (95% confidence interval, 3.4–11.3), respectively.ConclusionsThe majority of cardiac fatalities had evidence of both coronary heart disease and increased heart mass, and each condition was independently associated with a markedly elevated risk of cardiac death. Targeted screening for coronary heart disease, increased heart mass, and evidence of prior myocardial infarction should be considered to reduce duty‐related cardiac deaths among firefighters.

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Pathophysiologic Observations in Prehospital Ventricular Fibrillation and Sudden Cardiac Death

Cited by 306 publications

References 60 publications

Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.

Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.

Diverse mechanisms of unexpected cardiac arrest in advanced heart failure.

Pathoanatomic Findings Associated With Duty‐Related Cardiac Death in US Firefighters: A Case–Control Study

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