Homage to James B. Herrick: A Contemporary Look at Myocardial Infarction and at Sickle-Cell Heart Disease

James, Thomas N.

doi:10.1161/01.cir.101.15.1874

Cited by 33 publications

(17 citation statements)

References 86 publications

(68 reference statements)

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“…Moreover, because cardiac enzymes are released only when cardiomyocytes break down and cardiomyocytes typically rupture during necrosis but not apoptosis (13), evaluation of infarct size by cardiac enzyme values may underestimate the severity of myocardial infarction, especially in patients with predisposing conditions that may aggravate the magnitude of apoptosis. This explains our previous observation that the deleterious effect of dyslipidemia on postinfarct left ventricular systolic function was independent of the size of myocardial infarction estimated by cardiac enzyme changes (12).…”

Section: Figmentioning

confidence: 99%

“…Moreover, we previously demonstrated that the detrimental effect of hypercholesterolemia on postinfarct left ventricular ejection fraction is independent of the patency rate of infarct-related artery and the infarct size estimated by serum cardiac enzyme changes (12). Because cardiomyocyte apoptosis, which could not be evaluated by conventional serum cardiac enzyme changes (13), affects myocardial mechanics by reducing the force-generating capacity of the muscle, we speculated that hypercholesterolemia may increase the magnitude of cardiomyocyte apoptosis following ischemia and reperfusion and thereby aggravate the extent of postinfarct left ventricular systolic dysfunction.…”

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confidence: 99%

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Increased cardiomyocyte apoptosis following ischemia and reperfusion in diet‐induced hypercholesterolemia: Relation to Bcl‐2 and bax proteins and caspase‐3 activity

Wang

Chen

et al. 2002

Lipids

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It has been reported that apoptosis is a significant contributor to myocardial cell death as a result of reperfusion injury. However, whether the extent of cardiomyocyte apoptosis following ischemia and reperfusion varies in different pathophysiological backgrounds is still uncertain. In this study, we examined whether hypercholesterolemia increases the extent of myocardial reperfusion injury by aggravating cardiomyocyte apoptosis and the effects of hypercholesterolemia on the expression of Bcl-2 and Bax proteins and the activation of caspase-3. Twenty-eight male New Zealand white rabbits were fed standard chow (control, n = 14) or chow supplemented with 10% cholesterol (hypercholesterolemic, n = 14) for 8 wk. Anesthetized rabbits were then subjected to 30 min of left circumflex artery occlusion followed by 4 h of reperfusion. Apoptosis was identified as "DNA ladders" by gel electrophoresis and confirmed histologically using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay. The infarct size (% of risk region) was significantly greater in hypercholesterolemic rabbits than in controls (39 +/- 6 vs. 23 +/- 2%, P = 0.02). Very few TUNEL-positive cardiomyocytes could be identified in the nonischemic regions in both groups, consistent with an absence of DNA laddering. In contrast, TUNEL-positive cardiomyocytes were significantly displayed in the ischemic, nonnecrotic myocardium, and DNA ladder occurred in all animals. The percentage of TUNEL-positive cardiomyocytes in the ischemic nonnecrotic myocardium was significantly higher in hypercholesterolemic rabbits compared with controls (40 +/- 5 vs. 17 +/- 11%, P < 0.001). Western blot analysis showed that, in the nonischemic myocardium, hypercholesterolemic rabbits exhibited an approximately 50% increase in the expression of Bcl-2 (P < 0.05), but not Bax, than control rabbits. However, compared with controls, hypercholesterolemic rabbits exhibited a more pronounced decrease in the expression of Bcl-2 (42 +/- 4 vs. 26 +/- 2%, P < 0.01) and a similar extent of increase in the expression of Bax in the ischemic myocardium. Furthermore, hypercholesterolemic rabbits were associated with a markedly increased activation of caspase-3 within the ischemic myocardium compared to control rabbits. This study demonstrates that although hypercholesterolemia is associated with an increased myocardial Bcl-2/Bax ratio at baseline, it still significantly exacerbates cardiac reperfusion injury, not only by increasing the infarct size but also by increasing the extent of cardiomyocyte apoptosis.

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Section: Figmentioning

confidence: 99%

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confidence: 99%

Increased cardiomyocyte apoptosis following ischemia and reperfusion in diet‐induced hypercholesterolemia: Relation to Bcl‐2 and bax proteins and caspase‐3 activity

Wang

Chen

et al. 2002

Lipids

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“…219 1. Introduction James Bryan Herrick, an American physician was among the first to describe the symptoms of myocardial infarction (MI) (James, 2000). Herrick (1912) suggested, the symptoms and abnormalities of heart attacks was led by thrombosis in the coronary artery and this was not inevitable fatal.…”

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confidence: 99%

Diagnostics on acute myocardial infarction: Cardiac troponin biomarkers

Fathil

Arshad

Gopinath

et al. 2015

Biosensors and Bioelectronics

198

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“…Obrastzov and N.D. Strazhesko, in 1910 [4], and then by James B. Herrick in 1912 [5]. Herrick cited a German translation of the Russian article, and he reported that "myocardial infarction was not an inescapable tocsin of doom, but that it was often survived, sometimes with little lasting damage" [6]. Tables 1 and 2 present the classifications and definition of acute MI [7,8].…”

Section: Historymentioning

confidence: 99%