Comparison of Patients With Acute Myocardial Infarction With and Without Ventricular Fibrillation

Sudden cardiac arrest is a leading cause of death in industrialized countries, and ischemic ventricular fibrillation (VF) is a frequent cause.

The purpose of this study was to determine whether patients with ST elevation myocardial infarction (STEMI) who develop ischemic VF show more overall RR-interval irregularity (RRI) than do STEMI patients without ischemic VF.

Ischemic VF was identified in 41 patients from 1,473 digital 12-lead Holter recordings from three separate STEMI studies. Continuous 3-lead and 12-lead electrocardiogram (ECG) snapshots recorded every minute were compared between all ischemic VF patients and 123 random patients without ischemic VF. Time intervals from start of Holter to ischemic VF and equivalent intervals in the controls were used for calculations. ECG variables related to conduction intervals and severity of ischemia were measured using the most ischemic 12-lead ECG. RRI was calculated as the square root of the mean squared differences of successive RR intervals. For RRI, all QRS complexes, including ventricular ectopic beats, were used.

No baseline differences were observed between the study and control groups, except for male preponderance among ischemic VF patients (90% vs 72%, P = .019). QRS interval, ECG ischemia severity, RRI, and number of ventricular ectopic beats were significantly associated with ischemic VF. Multivariate analysis revealed RRI (odds ratio 1.006, 95% confidence interval 1.001–1.010, P = .016) and ST deviation score (odds ratio 1.073, 95% confidence interval 1.041–1.106, P <.001) as the only statistically significant predictors of ischemic VF.

In the period before ischemic VF, RRI and ST deviation score are associated with ischemic VF in STEMI patients. These findings could have important pathophysiologic and clinical implications.

The goal of this analysis was to evaluate the association of impaired Thrombolysis In Myocardial Infarction myocardial perfusion grade (TMPG) with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF).

Impaired TMPG after successful restoration of epicardial flow among patients treated with fibrinolytic therapy for ST-segment elevation myocardial infarction (STEMI) has been associated with adverse clinical outcomes, but its relationship to VT/VF has not been evaluated.

In the CLARITY-TIMI 28 (Clopidogrel as Adjunctive Reperfusion Therapy–Thrombolysis In Myocardial Infarction 28) study, 3,491 patients underwent angiography a median of 3.5 days after fibrinolytic administration for STEMI; TMPG was assessed, and its association with VT/VF was evaluated.

We observed VT/VF in 4.8% of patients. Impaired myocardial perfusion (TMPG 0/1/2) was associated with an increased incidence of VT/VF (7.1% vs. 2.6% with TMPG 3; log-rank p < 0.001). Among patients with restoration of normal epicardial flow (Thrombolysis In Myocardial Infarction flow grade 3), the incidence of VT/VF was increased among patients with impaired TMPG (4.7% vs. 2.7%; p = 0.02). Among patients with left ventricular ejection fraction ≥30%, impaired TMPG remained associated with an increased incidence of VT/VF (4.7% vs. 2.5%; p = 0.03). We found that VT/VF was associated with increased mortality (25.2% vs. 3.5%; p < 0.0001). Furthermore, among patients with VT/VF, impaired TMPG was associated with increased mortality (17.1% vs. 2.3%; p = 0.02). All but 1 death among patients who had VT/VF were among patients with impaired myocardial perfusion.

Despite restoration of normal epicardial flow or a left ventricular ejection fraction ≥30%, impaired myocardial perfusion on angiography 3.5 days after fibrinolytic administration for STEMI is associated with an increased incidence of VT/VF.

Acute myocardial infarction, often occurring postprandially, can be complicated by ventricular fibrillation. The role of acute alimentary lipemia and inflammation in the occurrence of ventricular arrhythmias in acute myocardial infarction has not been described yet.

Before and 2 h after consumption of a defined fatty meal, blood samples of 27 patients with a history of acute myocardial infarction (AMI) were incubated with lipopolysaccharide (LPS). In 10 patients, AMI was complicated by ventricular fibrillation (VF), in 17 patients, AMI occurred without VF. CD40-ligand and CD62P expression on platelets, tissue-factor binding on monocytes and platelet–monocyte aggregates were measured with flow cytometry. Soluble CD40-ligand plasma levels were measured with an ELISA.

With the meal, serum triglyceride levels increased from 211.85 ± 94.60 mg/dl to 273.59 ± 122.52 mg/dl (p = 0.0002). LPS stimulation before the meal showed a non-significant tendency to increase platelet–monocyte aggregates and tissue factor on monocytes in both patient groups. LPS stimulation in acute alimentary lipemia significantly increased tissue-factor expression on monocytes in both patient groups and platelet–monocyte aggregates in patients with VF. Baseline plasma levels of soluble CD40L did not differ significantly between both groups. Acute alimentary lipemia significantly decreased total plasma levels of sCD40L, leading to a significantly lower level of sCD40L in patients with a history of VF.

Alimentary lipemia enhances procoagulatory effects of inflammatory stimulation in patients with a history of AMI complicated by ventricular fibrillation. These observations might reveal a mechanism for an increased risk of VF in acute coronary syndromes in a postprandial state.

Although myocardial infarction (MI) severity is declining, the occurrence of ventricular arrhythmia (VA) after MI and its effect on outcome is unknown. This study was undertaken to examine the frequency and timing of VA and the effect of VA on mortality after MI.

Myocardial infarctions recorded between 1979 and 1998 were validated. Baseline characteristics, occurrence of VA, and survival were determined. Ventricular arrhythmias were categorized as primary ventricular fibrillation (VF), nonprimary VF, and ventricular tachycardia (VT). Logistic regression was used to analyze associations between VA and baseline characteristics. Temporal trends were assessed with the Mantel-Haenszel χ². Survival was analyzed with the Kaplan-Meier method. Proportional hazards regression was used to examine the association between death and occurrence of VA.

Among 2317 persons with incident MI, 7.5% experienced VA (3.6% nonprimary VF, 2.1% primary VF, 1.8% VT). Ventricular arrhythmia–associated factors were younger age, female sex, higher Killip class, ST elevation, and atrial fibrillation. Ventricular arrhythmias were associated with increased risk of death at 30 days.

Ventricular arrhythmias after MI are relatively common, particularly among persons with more severe MI and no prior history of coronary disease. Over time, the incidence of VF declined, whereas VT did not change. Ventricular arrhythmia after MI was associated with a 6-fold increase in morality. Thus, identification of high-risk MI survivors and prevention of VA could markedly improve outcomes. Further studies are needed to determine the cause of the shift in distribution of VA subtype.

Acute myocardial infarction can be complicated by ventricular arrhythmias due to electrophysiological changes in the ischemic myocardium, but the exact predisposing factors causing ventricular fibrillation during myocardial infarction still remain unclear. A role of inflammatory stimulation on platelets as a potential risk factor for ventricular fibrillation during acute myocardial infarction has not been described yet.

Whole blood samples of 21 patients with a history of acute myocardial infarction (AMI) and ventricular fibrillation (VF) were incubated with lipopolysaccharide (LPS). As a control group, we studied 19 patients without VF during AMI. CD40-ligand and CD62P expression on platelets and tissue factor binding on monocytes were measured by flow cytometry. Platelet–monocyte aggregates were measured by CD41 expression on platelets adherent to monocytes. Soluble CD40-ligand plasma levels were measured with an ELISA. Without LPS, no significant difference between the patient groups concerning CD40L expression on platelets was observed, but plasma levels of soluble CD40L were significantly higher in patients with a history of AMI with VF. After LPS stimulation, patients with a history of VF showed a significantly increased expression of CD40L in comparison to the patients without ventricular fibrillation, based on a significantly higher increase of CD40L expression. CD62P expression on platelets was significantly increased in patients with a history of VF.

Patients with a history of VF complicating AMI show an enhanced expression of CD40L on platelets after in vitro lipopolysaccharide-challenge with an enhanced platelet activation.

There are scarce and sometimes contradictory data about ventricular fibrillation (VF) during the acute phase of MI. In-hospital VF most often occurs with inferior MI, when treated with fibrinolytics. Out-of-hospital VF seems to be associated with anterior MI. We studied characteristics of patients with VF during reperfusion therapy by primary angioplasty (PCI) versus patients with VF before PCI.

From January 1995 until December 2001, we treated 2826 patients for acute MI and reviewed clinical records of all patients who developed VF and classified the patients according to the first episode of VF: either before or during the angioplasty procedure.

VF developed in 219 (8%) patients. Patients with VF during reperfusion therapy (n=74, 3%) were older (p=0.03), more frequently female (0.04), less often had heart failure (p=0.04), when compared with patient with VF before PCI (n=145, 5%). Patients with VF during PCI experienced more often preinfarction angina (p=0.009) and suffered more often from inferior MI (p=0.001), when compared with patients with VF before PCI.

Patients with early VF before reperfusion have different characteristics when compared with patients with VF during reperfusion. Infarct location is a major determinant of timing of VF, when both groups are compared (p<0.001).