Relevance of electrocardiographic findings, heart failure, and infarct site in assessing risk and timing of left ventricular free wall rupture during acute myocardial infarction

doi:10.1016/S0002-9149(99)80151-9

The American Journal of Cardiology

Volume 76, Issue 8, 15 September 1995, Pages 543-547

https://doi.org/10.1016/S0002-9149(99)80151-9 Get rights and content

Abstract

Clinical and electrocardiographic features of 227 patients who died of an acute myocardial infarction (AMI) were compared with those or 150 survivors of a first AMI. Left ventricular (LV) free wall rupture was found in 93 patients aged >50 years, but not in 134. The incidence of healed infarct (4 [4%] vs 50 [37%], p < 0.001), heart failure (11 [12%] vs 112 [84%], p < 0.001), and bundle branch block (11 [12%] vs 54 [40%], p < 0.001) was lower in patients with than without LV rupture. In patients with anterior AMI and early rupture (1 day), admission ST elevation was higher man in those with late LV rupture (>1 day, 6.8 ± 4.0 vs 4.0 ± 2.7 mm, p < 0.01). However, lateral wall AMI had minimal ST elevation and accounted for 10% of ruptures. On day 2, the decrease in ST segment in patients with late LV rupture was less than in survivors (0.5 ± 1.6 vs 3.2 ± 2.9 mm, p < 0.001). Admission systolic blood pressure in patients who had early rupture was higher than in survivors (155 ± 22 vs 137 ± 22 mm Hg, p < 0.001) and in those with late rupture (135 ± 23 mm Hg, p < 0.001). Late rupture was associated with infarct thinning and triggered by a physical strain in 18 of 45 patients (40%); infarct thinning, however, was present only in 4 of 48 patients (8%) with early rupture (p < 0.02). We conclude that (1) patients with LV rupture are among those >50 years of age with a first transmural AMI without conduction abnormalities or heart failure; (2) patients with anterior AMI, hypertension on admission, and high ST elevation are at risk for early rupture, whereas those without initial hypertension or high ST segment that remains elevated may have late rupture in an expanded infarction, often after an undue strain.

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Mechanical, inflammatory, and embolic complications of myocardial infarction: An emergency medicine review
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Citation Excerpt :
It is important to note, however, that the aforementioned findings vary with the location of infarction. The presence of an intraventricular conduction delay may be less prevalent in patients with VFWR, although the subsequent development of a new conduction delay may portend increased risk for rupture [28,36,40]. Echocardiography will demonstrate a pericardial effusion with signs of cardiac tamponade, including diastolic right ventricular collapse (high specificity), systolic right atrial collapse (earliest sign), a plethoric inferior vena cava with minimal respiratory variation (high sensitivity), and exaggerated respiratory cycle changes in mitral and tricuspid valve in-flow velocities as a surrogate for pulsus paradoxus [4,48].
Despite the declining incidence of coronary heart disease (CHD) in the United States, acute myocardial infarction (AMI) remains an important clinical entity, with many patients requiring emergency department (ED) management for mechanical, inflammatory, and embolic complications.
This narrative review provides an evidence-based summary of the current data for the emergency medicine evaluation and management of post myocardial infarction mechanical, inflammatory, and embolic complications.
While 30-day mortality rate after AMI has decreased in the past two decades, it remains significantly elevated at 7.8%, owing to a wide variety of subacute complications evolving over weeks. Mechanical complications such as ventricular free wall rupture, ventricular septal rupture, mitral valve regurgitation, and formation of left ventricular aneurysms carry significant morbidity. Additional complications include ischemic stroke, heart failure, renal failure, and cardiac dysrhythmias. This review provides several guiding principles for management of these complications. Understanding these complications and an approach to the management of various complications is essential to optimizing patient care.
Mechanical, inflammatory, and embolic complications of AMI can result in significant morbidity and mortality. Physicians must rapidly diagnose these conditions while evaluating for other diseases. In addition to understanding the natural progression of disease and performing a focused physical examination, an electrocardiogram and bedside echocardiogram provide quick, noninvasive determinations of the underlying pathophysiology. Management varies by presentation and etiology, but close consultation with cardiology and cardiac surgery is recommended.
Cardiac rupture in tako-tsubo cardiomyopathy with persistent ST-segment elevation
2012, International Journal of Cardiology
Post-infarct cardiac rupture: Recent insights on pathogenesis and therapeutic interventions
2012, Pharmacology and Therapeutics
Citation Excerpt :
However, when evaluating the clinical trend of a decline in rupture prevalence, one needs to be aware of the current extremely low rate of autopsy, which appears to be the only reliable way of confirming rupture diagnosis. In this regard, the percentage of autopsy-proven rupture out of total autopsied patients who died of acute MI has actually increased from under 10% during 1980s (Reddy & Roberts, 1989; Batts et al., 1990) to 12–65% in the recent decades, indicating the lack of effective strategies for rupture prevention (Figueras et al., 1995; Becker et al., 1999; Hutchins et al., 2002; Pouleur et al., 2010). In VALIANT trial, 24% of post-MI deaths were due to cardiac rupture confirmed by autopsy (Shamshad et al., 2010).
Ventricular wall rupture represents a catastrophic complication of myocardial infarction (MI) in the clinic while research has long been hampered due to absence of suitable animal models. Since late 1990s, the mouse has become a suitable model for human post-infarct cardiac rupture. Here we review the clinical features of post-infarct rupture, factors associated with a higher risk of rupture, and findings from clinical trials on the incidence of post-infarct rupture. The features of the mouse model of post-infarct cardiac rupture are discussed. Research using this model suggests acute ventricular remodeling as the fundamental change leading to rupture, and has defined several key factors that determine the risk of rupture. We then provide a comprehensive review of the progress of experimental research in this field focusing on recent findings from genetically modified mouse models and experimental therapeutic interventions that reveal molecular mechanisms of post-infarct rupture. Genetic and pharmacological interventions targeting key inflammatory mediators, regulatory factors of extracellular matrix collagen and healing process effectively reduced the risk of rupture. These findings convincingly demonstrate that cardiac inflammation, damage to extracellular matrix proteins or blunted fibrotic healing constitute the central mechanisms for the pathogenesis of cardiac rupture and acute ventricular remodeling. Studies using the mouse model have also identified novel molecular mechanisms and therapeutic targets as well as suitable interventional regimens providing useful clues for clinical translation.
Usefulness of leads V7, V8, and V9 ST elevation to diagnose isolated posterior myocardial infarction
2011, International Journal of Cardiology
Infarct size and post-infarct inflammation determine the risk of cardiac rupture in mice
2010, International Journal of Cardiology
Citation Excerpt :
Patients who died of rupture were more likely to have sustained hypertension, mental stress or physical strain, and usually had preserved LV function [3]. Figueras et al. [24] reported that the incidence of HF was lower in patients with than without subsequent rupture (12% vs. 84%). In addition, the ISIS-1 Trial showed that the β-antagonist atenolol reduced the risk of rupture implying a pro-rupture effect of the sympathoadrenergic activation, probably through hemodynamic enhancement [31].
Infarct size (IS) is a determinant of pathophysiological events after myocardial infarction (MI), but its relation to the risk of cardiac rupture remains undefined.
MI was induced in 129sv and C57Bl/6 mice. Left ventricular (LV) remodelling was examined by echocardiography prior to the onset of rupture. Changes in muscle tensile strength and expression of inflammatory factors were determined. Autopsy was performed and IS measured.
Rupture incidence was higher in 129sv than C57Bl/6 mice (62% vs. 33%, P < 0.001). Rupture occurred in mice with IS over a threshold, which was smaller in 129sv than C57Bl/6 mice (20% vs. 30%). 129sv mice with IS > 30% had a higher incidence of rupture than those with IS 20–30%. Echocardiography revealed IS-dependent LV remodelling and dysfunction and 129sv mice had a better-preserved function compared with C57Bl/6 counterparts. 129sv but not C57Bl/6 mice that subsequently developed rupture showed more severe regional dysfunction and remodelling compared with IS-matched non-ruptured hearts. Tensile strength of the infarcted myocardium was reduced significantly, which was IS-related. 129sv mice had higher expression levels of inflammatory mediators in the infarcted myocardium or circulating inflammatory cells, underlying the higher risk of rupture in this strain than C57Bl/6.
A critical IS level is necessary for post-MI rupture and IS correlates with the reduction in muscle tensile strength. Strain differences exist in global function and regional or systemic inflammation that explain the different risk of rupture or heart failure between strains. Limiting IS or minimizing inflammation would lower the risk of ventricular rupture.
Left Ventricular Free Wall Rupture After Acute Myocardial Infarction and Thrombolysis
2010, Dynamic Echocardiography

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Relevance of electrocardiographic findings, heart failure, and infarct site in assessing risk and timing of left ventricular free wall rupture during acute myocardial infarction

Abstract

Am J Cardiol

Am J Cardiol

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Am J Cardiol

Am J Cardiol

Hum Pathol

J Am Coll Cardiol

Chest

Am Heart J

Am J Cardiol

Am J Cardiol