The revised role of left ventricular dilatation and ACE-inhibition after myocardial infarction

It has generally been accepted that a myocardial infarction is complicated by extensive LVdilatation and that the main mechanism by which ACE-inhibitors produce their beneficial effects after myocardial infarction is attenuation of LV dilatation. This thesis tests both theories in an era where the primary prevention strategy after myocardial infarction has become the re-opening of the infarct related artery by administration of thrombolytic therapy or primary percutaneous coronary intervention (PCI). This thesis aims 1) to develop an adequate statistical model to describe the process of left ventricular (LV) dilatation after myocardial infarction, 2) to develop a prediction model to predict which patients are at risk of long-term LV dilatation, and 3) to investigate the effects of acute angiotensin converting enzyme (ACE) inhibitor treatment (administrated within 9 hours after myocardial infarction) on LV dilatation and clinical outcome in thrombolysed patients.

	titlepages/contents
	chapter 1
	chapter 2
	chapter 3
	chapter 4
	chapter 5
	chapter 6
	chapter 7
	dankwoord
	references
	samenvatting
	thesis

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