Gerald M. Pohost

American College of Cardiology/American Heart Association expert consensus document on electron-beam computed tomography for the diagnosis and prognosis of coronary artery disease

Coronary artery calcification is part of the development of atherosclerosis; it occurs exclusively in atherosclerotic arteries and is absent in the normal vessel wall. Electron-beam computed tomography (EBCT), the focus of this document, is a highly sensitive technique for detecting coronary artery calcium and is being used with increasing frequency for the screening of asymptomatic people to assess those at high risk for developing coronary heart disease (CHD) and cardiac events, as well as for the diagnosis of obstructive coronary artery disease (CAD) in symptomatic patients. The use of EBCT has the greatest potential for further determination of risk, particularly in elderly asymptomatic patients and others at intermediate risk. The calcium score has been advocated by some as a potential surrogate for age in risk-assessment models. EBCT has also been proposed as a useful technique for assessing the progression or regression of coronary artery stenosis in response to treatment of risk factors such as hypercholesterolemia. EBCT uses an electron beam in stationary tungsten targets, which permits very rapid scanning times. Serial transaxial images are obtained in 100 ms with a thickness of 3 to 6 mm for purposes of detecting coronary artery calcium. Thirty to 40 adjacent axial scans are obtained during 1 to 2 breath-holding sequences. Current EBCT software permits quantification of calcium area and density. Histological studies support the association of tissue densities of 130 Hounsfield units (HU) with calcified plaque. However, a plaque vulnerable to fissure or erosion can be present in the absence of calcium. Also, sex differences play a role in the development of coronary calcium, the prevalence of calcium in women being half that of men until age 60 years. EBCT calcium scores have correlated with pathological examination of the atherosclerotic plaque. This American College of Cardiology (ACC)/American Heart Association (AHA) Writing Group reviewed …

Patterns of haemodynamic alteration during left ventricular ischaemia in man. Relation to angiographic extent of coronary artery disease.

Haemodynamic changes produced by rapid atrial pacing (60 patients, 52 of whom developed angina) or in association with spontaneous angina (32 patients) were measured in 92 patients with angiographic coronary artery disease. The extent of coronary artery disease was scored by the jeopardy score system (range 0 to 12). The haemodynamic changes induced by ischaemia occurred in 3 patterns: pattern I, no change in filling pressure or in mean systemic arterial pressure; pattern II, a rise in filling pressure and a rise in mean systemic arterial pressure; pattern III, a rise in filling pressure, but no significant change or a fall in mean systemic arterial pressure. In patients who had a pattern II or a pattern III response to ischaemia, the change in mean systemic arterial pressure was linearly related to the corresponding change in cardiac output. The likelihood of a patient showing a given pattern of ischaemia-induced haemodynamic change was related to the extent of coronary artery disease; of 22 patients with jeopardy scores of 2 or 4, 91% exhibited pattern I, 9% pattern II, and none pattern III; of 39 patients with jeopardy scores of 6 or 8, 40% exhibited pattern I, 22% pattern II, and 38% pattern III; of 31 patients with jeopardy scores of 10 or 12, 12% exhibited pattern I, 10% pattern II, and 78% pattern III (P less than 0.01). Among the 54 patients in whom serial cardiac output determinations were available, a decline of the left ventricular function curve during ischaemia was demonstrable in 8% of those with a pattern I response, in 54% of those with a pattern II response, and in 90% of those with a pattern III response (P less than 0.01). The pattern of response was unrelated to resting angiographic left ventricular ejection fraction, whether ST segments became elevated or depressed, or whether ischaemia was pacing-induced or spontaneous. These results suggest that the haemodynamic response to ischaemia is determined by the fraction of the left ventricle that becomes dysfunctional during ischaemia.