Iterative reconstruction and individualized automatic tube current selection reduce radiation dose while maintaining image quality in 320-multidetector computed tomography coronary angiography.

AIM: To assess the effect of two iterative reconstruction algorithms (AIDR and AIDR3D) and individualized automatic tube current selection on radiation dose and image quality in computed tomography coronary angiography (CTCA). MATERIALS AND METHODS: In a single-centre cohort study, 942 patients underwent electrocardiogram-gated CTCA using a 320-multidetector CT system. Images from group 1 (n = 228) were reconstructed with a filtered back projection algorithm (Quantum Denoising Software, QDS+). Iterative reconstruction was used for group 2 (AIDR, n = 379) and group 3 (AIDR3D, n = 335). Tube current was selected based on body mass index (BMI) for groups 1 and 2, and selected automatically based on scout image attenuation for group 3. Subjective image quality was graded on a four-point scale (1 = excellent, 4 = non-diagnostic). RESULTS: There were no differences in age (p = 0.975), body mass index (p = 0.435), or heart rate (p = 0.746) between the groups. Image quality improved with iterative reconstruction and automatic tube current selection [1.3 (95% confidence intervals (CI): 1.2-1.4), 1.2 (1.1-1.2) and 1.1 (1-1.2) respectively; p < 0.001] and radiation dose decreased [274 (260-290), 242 (230-253) and 168 (156-180) mGy cm, respectively; p < 0.001]. CONCLUSION: The application of the latest iterative reconstruction algorithm and individualized automatic tube current selection can substantially reduce radiation dose whilst improving image quality in CTCA.

Determinants of coronary remodeling in transplant coronary disease: a simultaneous intravascular ultrasound and Doppler flow study.

BACKGROUND: Coronary remodeling plays a significant role in lumen loss in transplant allograft vasculopathy (TxCAD), but the determinants of remodeling are unknown. We assessed the relationship between remodeling and plaque topography, coronary compliance, and blood flow in TxCAD. METHODS AND RESULTS: One artery in each of 27 transplant patients was investigated with simultaneous intravascular ultrasound and coronary flow measurements (basal and hyperemic by Doppler flow wire). At 4 to 8 different cross sections (mean 5.1+/-1. 2), plaque topography (concentric or eccentric) was determined, and total vessel area, lumen area, and intimal/medial area (IMA) were measured. Mean remodeling ratio (vessel area/IMA) in eccentric lesions (E, n=28) was significantly larger than that in concentric lesions (C, n=70) (E 5.87+/-0.93 versus C 3.58+/-0.62; P<0.001), despite similar IMA (E 3.89+/-0.68 versus C 3.90+/-0.41; P=NS) and distribution of imaged segments. Remodeling ratio was consistently larger in eccentric lesions in all 3 vessel segments when analyzed separately, and mean remodeling ratio for each artery was larger in vessels with predominantly eccentric lesions. Coronary compliance ([Delta lumen area/diastolic lumen area]/Delta mean arterial pressure x 10(3)) was also significantly greater in eccentric lesions versus concentric lesions (proximal 1.00+/-0.39 versus 0.22+/-0.04; mid 0.71+/-0.17 versus 0.21+/-0.10; distal 0.43+/-0.13 versus 0. 01+/-0.08; all P<0.01). Coronary flow reserve was also significantly higher in coronary arteries with primarily eccentric lesions (E 2. 49+/-0.64 versus C 1.87+/-0.28; P<0.01). CONCLUSIONS: Vessel remodeling in transplant vasculopathy is significantly greater in eccentric lesions than in concentric lesions, possibly due to greater coronary compliance and resistive vessel function.

Impaired coronary tissue plasminogen activator release is associated with coronary atherosclerosis and cigarette smoking: direct link between endothelial dysfunction and atherothrombosis.

BACKGROUND: The aim of the study was to establish the influence of proximal coronary artery atheroma and smoking habit on the stimulated release of tissue plasminogen activator (tPA) from the heart. METHODS AND RESULTS: After diagnostic coronary angiography in 25 patients, the left anterior descending coronary artery (LAD) was instrumented, and the proximal LAD plaque volume was determined by use of intravascular ultrasound (IVUS). Blood flow and fibrinolytic responses to selective LAD infusion of saline, substance P (10 to 40 pmol/min; endothelium-dependent), and sodium nitroprusside (5 to 20 microgram/min; endothelium-independent) were measured by intracoronary IVUS and Doppler, combined with arterial and coronary sinus blood sampling. Mean plaque burden was 5.5+/-0.8 mm(3)/mm vessel (range 0.6 to 13.7 mm(3)/mm vessel). LAD blood flow increased with both substance P and sodium nitroprusside (P<0.001), although coronary sinus plasma tPA antigen and activity concentrations increased only during substance P infusion (P<0.006 for both). There was a strong inverse correlation between the LAD plaque burden and release of active tPA (r=-0.61, P=0.003). Cigarette smoking was associated with impaired coronary release of active tPA (current smokers, 31+/-23 IU/min; ex-smokers, 50+/-33 IU/min; nonsmokers 202+/-73 IU/min; P<0.05). CONCLUSIONS: We found that both the coronary atheromatous plaque burden and smoking habit are associated with a reduced acute local fibrinolytic capacity of the heart. These important findings provide evidence of a direct link between endogenous fibrinolysis, endothelial dysfunction, and atherothrombosis in the coronary circulation and may explain the greater efficacy of thrombolytic therapy for myocardial infarction in cigarette smokers.

Response of the pulmonary circulation to acetylcholine, calcitonin gene-related peptide, substance P and oral nicardipine in patients with primary pulmonary hypertension.

Endothelium-dependent vasodilation of the pulmonary vascular bed was investigated in five patients with primary pulmonary hypertension. Three endothelium-dependent vasodilators (acetylcholine, calcitonin gene-related peptide and substance P [in two patients]) were infused sequentially into the right atrium, followed by nicardipine given orally during full hemodynamic monitoring. Acetylcholine, calcitonin gene-related peptide and substance P had no effect on pulmonary artery pressure, total pulmonary vascular resistance or cardiac output, although calcitonin gene-related peptide significantly decreased systemic arterial systolic pressure from 132 +/- 34 to 113 +/- 33 mm Hg. In contrast, oral nicardipine decreased total pulmonary vascular resistance from 23 +/- 12 to 13 +/- 8 U, with a concomitant increase in cardiac output from 3.1 +/- 1 to 4.7 +/- 2 liters.min-1 and decrease in systemic vascular resistance from 30 +/- 9 to 13 +/- 4 U. Thus, despite the presence of a reversible component in these five patients with primary pulmonary hypertension, pulmonary vascular resistance did not decrease in response to the infused endothelium-dependent vasodilator agents, indicating that endothelium-dependent vasodilation is impaired in these patients.

Altered coronary vasodilator reserve and metabolism in myocardium subtended by normal arteries in patients with coronary artery disease.

OBJECTIVES: The aim of this study was to investigate coronary vasodilator reserve and metabolism in myocardium subtended by angiographically normal arteries remote from ischemia. BACKGROUND: After infarction, structural and functional changes occur in remote myocardium often subtended by normal arteries. Whether changes occur in regions remote from ischemic but noninfarcted myocardium is unknown. METHODS: Coronary vasodilator reserve was measured with positron emission tomography in 12 patients with single-vessel disease using intravenous dipyridamole (0.56 mg/kg for 4 min). In another 10 patients, simultaneous arterial/great cardiac vein catheterization was performed during atrial pacing to measure myocardial metabolism in regions subtended by diseased or normal arteries. RESULTS: Basal myocardial blood flow in stenosis-related regions was comparable to that in remote regions but was lower after dipyridamole administration (1.73 +/- 0.91 vs. 2.89 +/- 0.93 ml/min per g, p < 0.01), giving coronary vasodilator reserve values of 1.80 +/- 0.82 and 2.73 +/- 0.89 (p < 0.01). In normal control subjects, basal myocardial blood flow was 0.92 +/- 0.13 and 3.67 +/- 0.94 ml/min per g in the basal state and after dipyridamole (both p < 0.05 vs. values in remote regions), and coronary vasodilator reserve was 4.07 +/- 0.98 (p < 0.01) vs. values in remote regions). During pacing there was net lactate release in diseased regions (-18 +/- 27%, p < 0.05 vs. values in remote regions and control subjects) and extraction in remote regions (38 +/- 17%) and in normal control subjects (26 +/- 11%). Glucose and alanine extraction were increased in diseased (8 +/- 6% and 6 +/- 6%) and remote regions (6 +/- 3% and 4 +/- 3%), compared with values in normal control subjects (2 +/- 3% and -1 +/- 3%, both p < 0.05 vs. diseased and remote regions). CONCLUSIONS: Coronary vasodilator reserve is reduced and glucose and alanine metabolism is abnormal in regions subtended by normal arteries remote from ischemic but noninfarcted myocardium.

Delayed recovery of coronary resistive vessel function after coronary angioplasty.

OBJECTIVES: The aim of this study was to use Doppler catheterization and sequential dynamic positron emission tomography (PET) to investigate the role and time course of abnormal coronary resistive vessel function in the impairment of the coronary vasodilator response (maximal/basal coronary blood flow) after successful coronary angioplasty. BACKGROUND: The coronary vasodilator response may be impaired immediately after coronary angioplasty, despite successful dilation of a flow-limiting stenosis. METHODS: Twelve men (mean age 52 +/- 10 years) with single-vessel coronary artery disease and normal left ventricular function were studied. The coronary vasodilator response to intravenous dipyridamole (0.5 mg.kg-1 over 4 min) was determined from intracoronary Doppler measurement of coronary flow velocity, before and after successful angioplasty. Basal and maximal myocardial blood flow in the angioplasty region and a normal region were determined in nine patients wtih positron emission tomography with H2(15)0 at 1 day (PET1), 7 days (PET2) and 3 months (PET3) after angioplasty. RESULTS: The coronary vasodilator response, measured by Doppler catheterization, was similar before and immediately after angioplasty, 1.63 +/- 0.41 and 1.62 +/- 0.55, respectively (p = NS). After angioplasty, in seven of nine patients without restenosis, basal myocardial blood flow at PET1, PET2 and PET3 was 0.98 +/- 0.16, 0.94 +/- 0.09 and 0.99 +/- 0.13 ml.min-1 x g-1, respectively, in the remote region and 1.19 +/- 0.23 (p < 0.01 vs. remote region), 1.17 +/- 0.19 (p < 0.01 vs. remote region) and 1.10 +/- 0.08 ml.min-1 x g-1 (p = NS vs. remote region), respectively, in the angioplasty region. Myocardial blood flow after dipyridamole at PET1, PET2 and PET3 was 3.04 +/- 0.68, 3.00 +/- 0.71 and 3.00 +/- 0.60 ml.min-1 x g-1, respectively, in the remote region and 2.11 +/- 0.80 (p < 0.01 vs. remote region), 2.28 +/- 0.73 (p = NS vs. remote region) and 3.06 +/- 0.86 ml.min-1 x g-1 (p = NS vs. remote region), respectively, in the angioplasty region. The coronary vasodilator response at PET1, PET2 and PET3 was 3.15 +/- 0.85, 3.18 +/- 0.68 and 3.08 +/- 0.75, respectively, in the remote region and 1.80 +/- 0.68 (p < 0.01 vs. remote region), 1.94 +/- 0.49 (p < 0.01 vs. remote region) and 2.77 +/- 0.74 (p = NS vs. remote region), respectively, in the angioplasty region. CONCLUSIONS: After successful angioplasty, basal myocardial blood flow is increased for > or = 7 days in the angioplasty region, with a reduction in the dipyridamole-induced increase in maximal myocardial blood flow for > or = 24 h after the procedure. Thus, the coronary vasodilator response is impaired for > or = 7 days after angioplasty, indicating that there is abnormal resistive vessel function in the coronary vascular bed distal to a coronary artery stenosis that persists for 7 days to 3 months.

Diffuse reduction of myocardial beta-adrenoceptors in hypertrophic cardiomyopathy: a study with positron emission tomography.

OBJECTIVES: This study was conducted to determine the myocardial beta-adrenoceptor density as a marker of sympathetic function in patients with hypertrophic cardiomyopathy and normal control subjects. BACKGROUND: Although some cases of hypertrophic cardiomyopathy are familial with an autosomal dominant pattern of inheritance, there remains a substantial proportion of cases in which neither a family history nor genetic abnormalities can be demonstrated. Additional abnormalities, both genetic and acquired, may be important in the phenotypic expression of this condition. Clinical features of the disease and metabolic studies suggest an increased activity of the sympathetic nervous system. METHODS: Eleven patients with hypertrophic cardiomyopathy, none of whom had previously received beta-blocking drugs, and eight normal control subjects underwent positron emission tomography to evaluate regional left ventricular beta-adrenoceptor density and myocardial blood flow using carbon-11-labeled CGP 12177 and oxygen-15-labeled water as tracers. Plasma catecholamines were also measured. RESULTS: Mean (+/- SD) myocardial beta-adrenoceptor density was significantly less in the hypertrophic cardiomyopathy group than in the control group (7.70 +/- 1.86 vs. 11.50 +/- 2.18 pmol/g tissue, p < 0.001). Myocardial blood flow was similar in both groups (0.91 +/- 0.22 vs. 0.91 +/- 0.21 ml/min per g, p = NS). The distribution of beta-adrenoceptor density was uniform throughout the left ventricle in both groups. In the hypertrophic cardiomyopathy group, there was no correlation between regional wall thickness and myocardial beta-adrenoceptor density. There were no significant differences in either plasma norepinephrine or epinephrine concentrations between the two groups. CONCLUSIONS: There is a diffuse reduction in myocardial beta-adrenoceptor density in patients with hypertrophic cardiomyopathy in the absence of significantly elevated circulating catecholamine concentrations. This most likely reflects downregulation of myocardial beta-adrenoceptors secondary to increased myocardial concentrations of norepinephrine and is consistent with the hypothesis that cardiac sympathetic drive is increased in this condition.

Effect of intravenous calcitonin gene related peptide on ischaemia threshold and coronary stenosis severity in humans.

OBJECTIVE: Calcitonin gene related peptide (CGRP) is a potent vasodilator found in sensory nerve endings in coronary arteries. The effect of intravenous CGRP on myocardial ischaemia, cardiovascular haemodynamics, and epicardial coronary artery stenoses was studied in patients with angina to investigate the possible role of CGRP in the control of vasodilation in the coronary circulation. METHODS: 12 patients (mean age 60 years) performed exercise tests on consecutive days during intravenous infusions of placebo or CGRP (at 50 pmol.min-1). At cardiac catheterisation (6 patients), consecutive 20 min intravenous infusions of placebo and CGRP were given at a fixed heart rate, with measurement of haemodynamic variables and quantitative arteriography. RESULTS: The time to 0.1 mV ST depression increased from 475(SD 245) to 546(193) s (p < 0.05), and time to 0.2 mV ST segment depression, from 634(266) to 694(202) s (p < 0.05), on placebo and CGRP respectively. Rate-pressure product at 0.1 mV ST segment depression was 18,410(4590) and 20,750(7270) mm Hg.min-1 (p < 0.05), and at 0.2 mV ST depression it was 21,510(6470) and 24,080(7380) mm Hg.min-1 (p < 0.01), with placebo and CGRP, respectively. At catheterisation, diastolic blood pressure fell from 93(11) to 83(8) mm Hg (p < 0.05), systemic vascular resistance fell from 26.2(9.4) to 20.7(9.0) units (p < 0.05), and cardiac output increased from 5.94(1.10) to 6.73(1.04) litre.min-1 (p < 0.05), on placebo and CGRP respectively. Minimum luminal diameter increased from 0.66(0.23) to 1.11(0.15) mm (p < 0.01) with CGRP. CONCLUSIONS: Intravenous CGRP is a systemic arterial vasodilator which dilates coronary arteries at the site of atheromatous stenoses and delays the onset of myocardial ischaemia during treadmill exercise testing in patients with chronic stable angina.

Altered resistive vessel function after coronary angioplasty is not due to reduced production of nitric oxide.

BACKGROUND: The coronary vasodilator reserve with dipyridamole may be impaired immediately after successful angioplasty due to reduced endothelial production or release of nitric oxide. As the vasodilator response to exogenous nitrates is enhanced by endothelium removal or inhibition of nitric oxide synthesis, an increased vasodilator response to nitrovasodilators, such as nitroprusside, should occur. METHODS: The coronary vasodilator reserve (maximal/basel coronary blood flow) with intravenous dipyridamole (0.56 mg/min for 4 min) was measured by Doppler catheterization before and after angioplasty in 10 patients with single-vessel coronary disease. At peak dipyridamole effect, incremental doses of nitroprusside (4-50 micrograms/min) were given intracoronary until systolic blood pressure fell by > or = 5 mmHg. RESULTS: Before angioplasty, the coronary blood flow increased from 19.7 +/- 6.1 (mean +/- s.d.) at basal to 30.1 +/- 11.9 ml/min at the peak dipyridamole effect (P < 0.01), giving a coronary vasodilator reserve of 1.62 +/- 0.39 (range 1.20 - 1.96). After angioplasty, the coronary blood flow increased from 32.4 +/- 13.2 at basal to 53.4 +/- 23.3 ml/min at the peak dipyridamole effect (P < 0.01), giving a coronary vasodilator reserve of 1.77 +/- 0.64 (range 1.7-2.42). Sodium nitroprusside had no additional effect on coronary flow (49.5 +/- 20.4 and 52.2 +/- 18.0 ml/min) before and after a fall in systolic blood pressure, respectively. CONCLUSIONS: The vasodilator response to dipyridamole was markedly impaired immediately after successful angioplasty, and was not augmented by intracoronary nitroprusside. Thus, a reduced production or release of nitric oxide in the coronary circulation does not seem to be responsible for the impaired vasodilator response after angioplasty.

Plasma levels of active Von Willebrand factor are increased in patients with first ST-segment elevation myocardial infarction: a multicenter and multiethnic study.

AIMS: Von Willebrand factor (VWF), a key player in hemostasis and thrombosis, is released from endothelial cells during inflammation. Upon release, VWF is processed by ADAMTS13 into an inactive conformation. The aim of our study was to investigate whether plasma levels of active VWF, total VWF, ADAMTS13, osteoprotegerin (OPG) and the ratios between VWF and ADAMTS13 are risk factors for first ST-segment elevation myocardial infarction (STEMI). METHODS AND RESULTS: We assessed 1026 patients with confirmed first STEMI and 652 control subjects from China, Italy and Scotland, within six hours after their cardiovascular event. Median plasma levels of total VWF, active VWF, OPG and ratios VWF/ADAMTS13 were increased, while plasma levels of ADAMTS13 were decreased in patients compared to controls. The odds ratio (OR) of STEMI in patients with high plasma levels of active VWF was 2.3 (interquartile range (IQR): 1.8-2.9), total VWF was 1.8 (1.4-2.3), ADAMTS13 was 0.6 (05-0.8), OPG was 1.6 (1.2-2.0) and high VWF/ADAMTS13 ratios was 1.5 (1.2-2.0). The OR for total VWF, active VWF and ratios VWF/ADAMTS13 remained significant after adjustment for established risk factors, medical treatment, C-reactive protein, total VWF, ADAMTS13 and OPG. When we adjusted for levels of active VWF, the significance of the OR for VWF and ratios VWF/ADAMTS13 disappeared while the OR for active VWF remained significant. CONCLUSIONS: We found evidence that plasma levels of active VWF are an independent risk factor for first STEMI in patients from three different ethnic groups. Our findings confirm the presence of VWF abnormalities in patients with STEMI and may be used to develop new therapeutic approaches.

Effect of aging on myocardial perfusion reserve.

UNLABELLED: Myocardial perfusion reserve (hyperemic divided by basal myocardial blood flow) describes vasodilator responsiveness of coronary-resistive vessels. The effect of aging and gender on myocardial perfusion reserve remains controversial. METHODS: We studied 56 normal volunteers (21 women, 35 men; aged 50 +/- 20 yr, range 21-86 yr) with 15O-water PET to measure myocardial blood flow during basal and hyperemic states with intravenous dipyridamole (0.56 mg/kg, n = 46) or adenosine (140 micrograms/kg/min, n = 10). For comparative analysis, patients were grouped according to age: < 30 yr (n = 11), 30-49 yr (n = 18), 50-69 yr (n = 15) and > or = 70 yr (n = 12). RESULTS: Overall, basal flow was 1.00 +/- 0.26 ml/min/g and hyperemic flow was 3.31 +/- 1.38 ml/min/g, resulting in a myocardial perfusion reserve of 3.38 +/- 1.35. There was an increase in basal flow with age (r = 0.45, p < 0.025), although hyperemic flow was only lower in patients > or = 70 yr, causing a significant reduction in myocardial perfusion reserve: 3.54 +/- 0.96 in < 30 yr, 4.23 +/- 1.35 in 30-49 yr, 3.51 +/- 1.21 in 50-69 yr and 1.94 +/- 0.46 in > or = 70 yr (p < 0.05 versus all groups < 70 yr). CONCLUSION: Myocardial blood flow during basal and hyperemia conditions are roughly comparable up to 60 yr of age. Above this age, there is significant increase in basal flow associated with an increase in systolic blood pressure. Above 70 yr, there is a significant reduction in hyperemic flow, and thus myocardial perfusion reserve independent of hemodynamic response to vasodilator stress.

Impairment of the myocardial vasomotor response to cold pressor stress in collateral dependent myocardium.

OBJECTIVE: To study the vasomotor response (cold pressor/basal flow) in myocardium perfused entirely by collaterals, using the reflex sympathetic stimulation of cold pressor stress. DESIGN: Regional myocardial blood flow was measured in collateral dependent and in remote myocardium using positron emission tomography with 15O water at basal and at cold pressor stress. Regional ischaemia was measured with 18F-fluorodeoxyglucose (FDG). PATIENTS: Nine patients (mean (SD) age 53 (6) years) with an occluded coronary artery supplied entirely by collaterals from other angiographically normal arteries. RESULTS: In remote myocardium, basal and cold pressor flow were 0.99 (0.26) and 1.46 (0.60) ml/min/g (P < 0.05), respectively, a myocardial vasomotor response of 1.46 (0.45). In collateral dependent myocardium, basal and cold pressor flow were 0.91 (0.20) and 0.87 (0.35) ml/min/g, respectively (the latter value, P < 0.05 v remote region), a myocardial vasomotor response of 0.97 (0.43) (P < 0.05 v remote region). The myocardial vascular resistance (mean arterial pressure/flow) during cold pressor was higher in the collateral dependent than in remote myocardium, at 147.0 (61.1) and 85.6 (32.3) mm Hg.min.g/ml (P < 0.05), respectively, but with no relative increase in FDG uptake. CONCLUSIONS: In contrast to the decrease in myocardial resistance in remote myocardium with cold pressor, an increase was observed in collateral dependent myocardium suggesting a vasoconstrictor response in resistive vessels, without demonstrable myocardial ischaemia.

The progression of thrombus in an ex-vivo shunt model evaluated by intravascular ultrasound radiofrequency analysis.

We tested the ability of ultrasound radiofrequency (RF) signal analysis to characterize thrombus accumulation in a Dacron graft incorporated into the exteriorized arteriovenous shunt in 3 baboons with constant blood flow for 60 min. Thrombus formation was quantified by sequential measurements of 111Indium-labeled platelet deposition. RF signals were acquired every 15 min at 2 sites in the graft, using a 2.9 Fr intravascular ultrasound catheter-based transducer (30 MHz) and digitized at 250 MHz in 8-bit resolution. Regions of interest were placed within a 0.5-mm perimeter adjacent to the graft wall. Integrated backscatter increased significantly (p < 0.001) with increasing platelet deposition. However, mean-to-standard deviation ratio of the RF envelope showed no significant change and the distribution pattern of the RF probability function remained constant and consistent with a Rayleigh scattering process. These results provide a basis for using RF analysis to monitor the time-course of thrombus formation.

Myopericarditis in Churg-Strauss syndrome.

Churg-Strauss syndrome is a disseminated vasculitis with multisystem involvement, characterized by necrotizing arteritis, eosinophilic infiltration, and extravascular granuloma formation. In as many as 60% of all cases, the heart may be affected. We describe a 30-year-old man in whom pericarditis was followed by the development of a large pericardial effusion, with evidence of impaired right and left ventricular function. The patient had a 5-year history of asthma. Early therapy with high-dose prednisolone and azathioprine led to resolution of the pericardial effusion and prevented a further reduction in biventricular function.

Cardiac and coronary CT comprehensive imaging approach in the assessment of coronary heart disease.

Cardiac CT is a rapidly advancing technology. Non-invasive CT coronary angiography is an established technique for assessing coronary heart disease with accuracy similar to invasive coronary angiography. CT myocardial perfusion imaging can now identify perfusion defects in animal models and humans. MRI is the current 'gold standard' for the assessment of myocardial viability, but it is now also possible to assess delayed enhancement by CT. This has led to the possibility of a 'one-stop shop' for cardiovascular imaging that would provide information on anatomy, function, perfusion and viability in one rapid diagnostic test at a radiation dose equivalent to contemporary nuclear medicine imaging. This review discusses the current status of 'one-stop shop' cardiac CT assessment, clinical utility and directions for future research.