Is the Beneficial Effect of Preinfarction Angina Related to an Immune Response?

Abstract

SUMMARYImmune-mediated mechanisms are thought to play a key role in the development of coronary artery disease and its thrombotic complications. Preinfarction angina has been suggested to improve left ventricular function and short-term outcomes.The purpose of the present study was to investigate the relation between the immune response and in-hospital clinical course in preinfarction angina.We prospectively evaluated 93 patients. Forty-three patients exhibited preinfarction angina within 24 hours before the onset of acute myocardial infarction (AMI) (preinfarction angina group) and 50 patients were free from preinfarction angina (sudden onset group). The incidence of complications (heart failure, recurrent angina, arrhythmia and coronary interventions) and in-hospital mortality were assessed in the two study groups. We detected some immune markers, including white blood cells, C-reactive protein, immunoglobulins, and complement.White blood cells and CRP were significantly lower in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.005, respectively). Conversely, IgE and C 4 were significantly higher in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.001, respectively). The incidences of heart failure and severe arrhythmias were lower in the preinfarction group than in the sudden onset group (P < 0.005, P < 0.05 respectively).The beneficial effect of preinfarction angina may be associated with an immuneinflammatory response modified by a brief ischemic episode. (Jpn Heart J 2004; 45: 205-215)

Interaction of Cardiovascular Risk Factors with Myocardial Ischemia/Reperfusion Injury, Preconditioning, and Postconditioning

“…In patients, ischemic preconditioning, as indicated by preinfarction angina within 24 h before infarction, reduces infarct size and left ventricular remodeling, thereby potentially improving the prognosis of patients with an acute myocardial infarction (Anzai et al, 1995;Kloner et al, 1995;Kloner et al, 1998b;Papadopoulos et al, 2003;Yellon and Downey, 2003;Solomon et al, 2004;Tokac et al, 2004). When preinfarction angina occurred within 48 h before acute myocardial infarction, no such difference in irreversible tissue injury and outcome was measured compared with patients without any ischemic symptoms before infarction (Psychari et al, 2004).…”

Serum IgE levels in coronary artery disease

“…It was concluded that the level of IgE significantly increased during the acute phase of acute coronary syndromes and gradually decreased, supporting the role of acute inflammatory response and mast cell involvement in plaque rupture. 5 The incidence of complications (heart failure, recurrent angina, arrhythmia and coronary interventions) and in-hospital mortality were prospectively assessed in two study groups [9] consisting of 43 patients with preinfarction angina, within 24 h before the onset of acute myocardial infarction (preinfarction angina group), and 50 patients without preinfarction angina (sudden onset group). White blood cells and CRP were significantly lower in the preinfarction angina group than in the sudden onset group.…”

Risk of Cardiovascular Mortality in Relation to Increased Total Serum IgE Levels in Older Adults: A Population-Based Cohort Study

“…Criqui et al (1987) reported the first results in a population-based study showing a significant positive association between total IgE levels and cardiovascular diseases (i.e., previous myocardial infarction, stroke, and noninvasively diagnosed large-vessel peripheral arterial disease) in males [15]. Subsequent cross-sectional studies reported increased total IgE levels in patients with AMI, coronary heart disease, and angina compared with healthy counterparts or controls [8,9,10,16]. Using the same data from NHANES 2005–2006 as in the present study, Shiue et al (2013) investigated the effect of total serum and 19 allergen-specific IgE levels with regard to self-reported cardiovascular events, including coronary heart disease, stroke, heart failure, heart attack, and angina [14].…”

“…The proposed mechanism is both IgE-independent and -dependent, and involves mast cells that trigger the release of vasoactive inflammation mediators, contributing to the development and progression of myocardial ischemia and thrombosis [5,6,7]. Several cross-sectional studies have demonstrated elevated total serum IgE levels in patients with acute myocardial infarction (AMI), sudden cardiac arrest, and coronary artery disease [8,9,10]. A few prospective studies have suggested elevated total IgE levels as an independent marker of AMI development [11,12].…”