Sensitivity, specificity and accuracy of stress SPECT myocardial perfusion imaging for detection of coronary artery disease in the distribution of first-order branch vessels, using an anatomical matching of angiographic and perfusion data.

We sought to investigate the utility of stress single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) for the identification of coronary artery disease (CAD) in the distribution of first-order branch vessels. We evaluated 135 consecutive patients with coronary angiography and stress SPECT MPI. We anatomically matched angiography and SPECT to assess the sensitivity, specificity and accuracy of SPECT MPI for the detection of CAD in the distribution of first-order branches. Subgroup analysis for stress test performance and previous coronary artery bypass grafting (CABG) was also performed. The sensitivity, specificity and accuracy of stress SPECT MPI for the detection of CAD in the distribution of first-order branch vessels were all 67%. For isolated branch vessel CAD, stress SPECT MPI had a sensitivity of 44%. In patients without CABG, the sensitivity, specificity and accuracy for the detection of CAD in the distribution of first-order branch vessels were 71%, 67% and 68%, compared with 60%, 67% and 64% for patients with CABG. The sensitivity for isolated branch vessel CAD was 50% for patients without CABG, but only 29% for patients with CABG. The sensitivity and specificity for CAD in the distribution of branch vessels were similar for all patients for all stress test modalities and heart rate response (sensitivity, 64-69%; specificity, 61-69%). Stress SPECT MPI offers intermediate sensitivity, specificity and accuracy for the detection of CAD in the distribution of first-order coronary artery branch vessels. However, for isolated branch vessel CAD, stress SPECT has a lower sensitivity, particularly in patients with previous CABG.

Validation of a model of left ventricular segmentation for interpretation of SPET myocardial perfusion images.

Several models of left ventricular segmentation have been developed that assume a standard coronary artery distribution, and are currently used for interpretation of single-photon emission tomography (SPET) myocardial perfusion imaging. This approach has the potential for incorrect assignment of myocardial segments to vascular territories, possibly over- or underestimating the number of vessels with significant coronary artery disease (CAD). We therefore sought to validate a 17-segment model of myocardial perfusion by comparing the predefined coronary territory assignment with the actual angiographically derived coronary distribution. We examined 135 patients who underwent both coronary angiography and stress SPET imaging within 30 days. Individualized coronary distribution was determined by review of the coronary angiograms and used to identify the coronary artery supplying each of the 17 myocardial segments of the model. The actual coronary distribution was used to assess the accuracy of the assumed coronary distribution of the model. The sensitivities and specificities of stress SPET for detection of CAD in individual coronary arteries and the classification regarding perceived number of diseased coronary arteries were also compared between the two coronary distributions (actual and assumed). The assumed coronary distribution corresponded to the actual coronary anatomy in all but one segment (#3). The majority of patients (80%) had 14 or more concordant segments. Sensitivities and specificities of stress SPET for detection of CAD in the coronary territories were similar, with the exception of the RCA territory, for which specificity for detection of CAD was better for the angiographically derived coronary artery distribution than for the model. There was 95% agreement between assumed and angiographically derived coronary distributions in classification to single- versus multi-vessel CAD. Reassignment of a single segment (segment #3) from the LCX to the LAD territory further improved the model's fit with the anatomic data. It is concluded that left ventricular segmentation using a model with assumed coronary artery distribution is valid for interpretation of SPET myocardial perfusion imaging.

Disparate effects of ACE-inhibitors and calcium antagonists on left ventricular structure and function in essential hypertension.

The present study was designed to compare the effects of angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists-the two drug classes thought to be most effective in reducing left ventricular hypertrophy-on arterial pressure, left ventricular structure and function in patients with essential hypertension. After a placebo period of 4 weeks, a population of 96 patients were treated either with one of five different ACE inhibitors or one of six different calcium antagonists. Cardiac structure and function was assessed by 2D-guided M-mode echocardiography. Whereas both drug classes lowered arterial pressure to the same extent, ACE inhibitors had a more pronounced effect on posterior and septal wall thickness and left ventricular mass index than calcium antagonists. Diastolic function, as measured by peak filling rate and duration of rapid filling, improved in both treatment groups to the same extent. However, systolic performance, as assessed by midwall fractional fibre shortening, was significantly improved by ACE inhibitors only. Myocardial contractility (end-systolic wall stress/end-systolic volume index) showed no significant change in the ACE inhibitor group but decreased after treatment with calcium antagonists. We conclude that both calcium antagonists and ACE inhibitors lower arterial pressure and increase left ventricular filling to the same extent. However, compared with calcium antagonists, ACE inhibitors had a more pronounced effect on left ventricular mass and improved systolic ventricular performance in patients with essential hypertension.

Cardiovascular effects of a trandolapril/verapamil combination in patients with mild to moderate essential hypertension.

The cardiovascular effects of a combination of trandolapril and verapamil were evaluated in 14 patients with mild to moderate essential hypertension. This combination therapy decreased arterial pressure mainly through a decrease in total peripheral resistance without causing an increase in heart rate or cardiac output: left ventricular mass was significantly reduced, cardiac systolic function improved, and plasma volume and renal blood flow remained unchanged.

Hypertension and left-ventricular hypertrophy.

Left-ventricular hypertrophy (LVH), the primary cardiac manifestation of hypertension, has been identified as the most powerful risk factor for future cardiovascular events causing morbidity and mortality, such as myocardial infarction, congestive heart failure, sudden death, and so forth. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left-ventricular filling and contractility. Besides hypertension, other risk factors such as obesity, advanced age, valvular heart disease, and other pathologic disorders can cause an increase in the hemodynamic burden and lead to LVH. Nonhemodynamic determinants of left-ventricular mass include dietary salt intake, alcohol, and neurohormones. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.

Activation of phospholipase A2 by 1,25 (OH)2 vitamin D3 and cell growth in monocytic U937 and Mono Mac 6 cells.

Soluble phospholipase A2 activity was characterized in two human monocytic cell lines, U937 and Mono Mac 6. The enzyme showed an absolute requirement for Ca++, an alkaline pH optimum and Michaelis-Menten kinetics in both cell lines. Differentiation of U937 and Mono Mac 6 cells with 1,25 (OH)2 vitamin D3 (10 nM, 72 h) enhanced PLA2 activity by 82 per cent and 56 per cent, respectively. Furthermore, kinetic experiments revealed that enzyme activity increased within 3 h when cells were brought from the nonproliferative phase of growth to the start of a new cycle of cell proliferation. This initial activation of PLA2 could be inhibited by cycloheximide and actinomycin D, indicating the requirement of gene transcription. Taken together, these results suggest a role of cytosolic, Ca(++)-dependent PLA2 in differentiation and growth of monocytic cells.