Clinical Significance
Coronary Perfusion Pressure in Cardiovascular Disease
CPP becomes reduced in common cardiac conditions, including heart failure and coronary artery disease; patients with these conditions are more prone to myocardial ischemia.
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The impaired ejection of blood from the left ventricle defines systolic heart failure; this increases LVEDP, and thus CPP and left ventricular perfusion are reduced.[9] LVEDP also increases in diastolic heart failure.[10] Compensatory increases in sympathetic drive initially increase myocardial contractility and blood pressure, which increases aortic diastolic pressure to maintain systemic and coronary blood flow.[11] However, increases in systolic blood pressure also increase cardiac afterload and promote cardiac remodeling. Therefore, myocardial oxygen demand increases due to hypertrophy of the myocardium and increased afterload on a background of raised LVEDP; the myocardium will be vulnerable to ischemia.[9][10][11]
Atherosclerotic plaques causing stenosis of coronary vessel lumens characterize coronary artery disease. Plaques impede flow through coronary circulation, necessitating compensatory coronary vasodilation distal to the plaque to maintain coronary flow and myocardial oxygen delivery. As stenosis progresses, the coronary flow becomes dependent on CPP. Myocardial ischemia occurs when CPP is unable to sustain coronary perfusion as autoregulation fails.[7][12] Myocardial infarction resulting from reduced coronary perfusion will be a topic of discussion below.[7][12]
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Coronary Perfusion Pressure in Type 2 Myocardial Infarction
Type 1 myocardial infarction implies the rupture of a coronary atherosclerotic plaque with subsequent thrombus formation and stenosis of the arterial lumen.[13] Type 2 myocardial infarction occurs independently from coronary atherosclerotic plaque rupture instead of resulting from an imbalance in myocardial oxygen supply and demand. Decreased myocardial oxygen delivery may be caused by hypotension with reduced CPP, systemic hypoxia, or anemia. Increased myocardial oxygen demand may result from increased afterload or tachyarrhythmia. Type 2 myocardial infarction may be multifactorial; for example, tachyarrhythmia may increase oxygen demand and reduce stroke volume with subsequent hypotension and reduced CPP. According to the physiologic principles discussed above, patients with pre-existing cardiac disease, including coronary artery disease and myocardial hypertrophy, are reliant on CPP, so are less tolerant of reduced CPP and decreased myocardial oxygen delivery.[13]
Type 1 and 2 myocardial infarctions are associated with similar mortality rates [14]. However, while protocolized management of type 1 myocardial infarction has improved outcomes in recent decades, difficulties exist regarding the management of type 2 myocardial due to a lack of accepted definitions and treatment. Acute management involves the restoration of blood pressure and, thus re-establishment of CPP. This article will discuss the therapeutic modification of CPP by pharmacological and mechanical therapies will be discussed below.[14]
Therapeutic Modification of Coronary Perfusion Pressure
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Two examples of therapies that modify CPP are glyceryl trinitrate and the intra-aortic balloon pump (IABP).
Glyceryl trinitrate is an agent used in the acute management of type 1 myocardial infarction. Studies have shown that low-dose glyceryl trinitrate administration reduces LVEDP without reducing aortic diastolic pressure, thus increasing CPP.[15] The predominant action of Glyceryl trinitrate is central venous dilatation, which reduces cardiac preload; this reduces stroke volume according to the Frank-Starling law, and therefore, myocardial oxygen demand decreases.[16][15]
The IABP is the most commonly used form of mechanical support in the acutely failing heart.[17] It is placed percutaneously and sits in the descending aorta distal to the aortic arch. Inflation occurs during diastole, which increases aortic diastolic blood pressure to increase CPP and augment myocardial oxygen delivery. LVEDP and cardiac afterload are reduced, which decreases myocardial oxygen demand. IABPs, therefore, simultaneously increase myocardial oxygen supply and decreased oxygen demand.[17]
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