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Chapter 1

The Thrombotic AMI Lesion: Lessons from Pathology more...

Chapter 2

Electrocardiographic Identification of the Culprit Lesion in ST-Segment Elevation Myocardial more...

Chapter 3

The Role of Thrombolysis in the Era of STEMI Interventions more...

Chapter 4

STEMI Interventions: A Review of Relevant Clinical Trials more...

Chapter 5

Updated Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction more...

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Chapter 1
The Thrombotic AMI Lesion: Lessons from Pathology
Masataka Nakano, MD, Marc Vorpahl, MD, Saami Yazdani, PhD, Elena Ladich, MD, Robert Kutys, MS, Frank D. Kolodgie, PhD, and Renu Virmani, MD

Introduction
Atherosclerosis is a pathologically diverse disease with heterogeneous risk factors, genetic predispositions and mechanisms of progression. Given the definitions used for inclusion of early lesions of atherosclerosis, this disease affects all even relatively young populations, but usually manifests in middle age.

Nearly 70% of the morbidity and mortality from coronary disease is the result of thrombosis secondary to plaque rupture, which generally does not occur until the fourth decade of life. Less common attributions of thrombosis include plaque erosion and calcified nodules. More than 95% of acute myocardial infarcts are the result of coronary atherosclerosis with superimposed luminal thrombus, sometimes designated as atherothrombosis. Uncommon causes of myocardial infarction include coronary spasm, coronary embolism, coronary vasculitis, coronary dissections, congenital abnormal origin of coronary arteries, and thrombosis in non-atherosclerotic normal vessels. Additionally, concentric subendocardial necrosis may result from global ischemia in the presence of poor cardiac
output in cases of prolonged cardiac arrest with resuscitation.

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