The association between early ventricular arrhythmias, renin-angiotensin-aldosterone system antagonism, and mortality in patients with ST-segment-elevation myocardial infarction: Insights from Global Use of Strategies to Open coronary arteries (GUSTO) V.
BACKGROUND
The long-term prognostic significance of early (<48 hours) ventricular fibrillation (VF) or sustained ventricular tachycardia (VT) in patients with an acute myocardial infarction remains controversial. Emerging data suggest that some of the benefit of renin-angiotensin-aldosterone system (RAAS) antagonism may be derived from a reduction in the incidence of these arrhythmias in the setting of acute myocardial infarction.


METHODS
We assessed the relationship between early VF/VT (defined as within 48 hours after admission) and mortality in 16,588 patients from global use of strategies to open coronary arteries (GUSTO) V trial. Furthermore, we examined the relationship between baseline use of angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB), early VF/VT, and mortality.


RESULTS
Early VF or VT occurred in 732 (4.4%) patients. Compared to patients without VF/VT, those experiencing early VF or VT had a significant increase in 30-day mortality (22% vs 5%, P < .001). Baseline use of an ACEI/ARB was associated with a decreased incidence of early VF/VT (odds ratio 0.65, 0.47-0.89, P = .008). A lower 30-day mortality was seen in patients with early VF/VT on baseline ACEI/ARB compared with patients with early VF/VT not receiving an ACEI/ARB at baseline (17.7% vs 24.2%, respectively, P = .04). The association between baseline RAAS antagonism and mortality persisted after adjustment for multiple confounders.


CONCLUSIONS
In patients presenting with acute myocardial infarction, early VF/VT identifies those at increased risk for 30-day mortality. Baseline use of RAAS antagonists is associated with a reduced incidence of malignant arrhythmias. Identifying how this association impacts short-term mortality in this patient population requires further prospective evaluation.
Askari
Arman T
AT
Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH, USA. arman.askari64@gmail.com
Shishehbor
Mehdi H
MH
Kaminski
Matthew A
MA
Riley
Michael J
MJ
Hsu
Amy
A
Lincoff
A Michael
AM
D000077284:Abciximab; D000368:Aged; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D000925:Anticoagulants / Q000008:administration & dosage; D004359:Drug Therapy, Combination; D023381:Endpoint Determination; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000401:mortality*; D011379:Prognosis; D016016:Proportional Hazards Models; D011994:Recombinant Proteins / Q000008:administration & dosage; D018570:Risk Assessment; D017180:Tachycardia, Ventricular / Q000209:etiology; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage; D014693:Ventricular Fibrillation / Q000209:etiology
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D005343:Fibrinolytic Agents; D007140:Immunoglobulin Fab Fragments; D011994:Recombinant Proteins; C087896:reteplase; D010959:Tissue Plasminogen Activator; D000077284:Abciximab