Coronary artery bypass graft imaging using ECG-gated multislice computed tomography: comparison with catheter angiography.

AIM: To compare the value of multislice computerized tomography (MSCT) in imaging coronary artery bypass grafts (CABGs) by direct quantitative comparison with standard invasive angiography. METHODS: Using MSCT, 50 consecutive patients who had previously undergone CABG surgery and had recently undergone invasive angiography for recurrent angina pectoris, were studied further using MSCT after intravenous injection of non-ionic contrast agent; cardiac imaging was performed during a single breath-hold. Graft anatomy was quantified, using both quantitative coronary angiography (QCA) and MSCT, by different investigators blinded to each other. Reproducibility was quantified using the standard error of the measurement expressed as a percentage in log-transformed values (CV%) and intraclass correlation (ICC). RESULTS: All 150 grafts were imaged using MSCT; only 4 patent grafts were not imaged using selective angiography. Good agreement was achieved between MSCT and QCA on assessment of proximal anastomoses (CV% 25.2, ICC 0.84), mid-vessel luminal diameter (CV% 15.5, ICC 0.91) and aneurysmal dilations (CV% 14.3). Reasonable agreement was reached on assessment of distal anastomoses (CV% 26.7, ICC 0.66) and categorization of distal run-off (ICC 0.73). Good agreement was observed for stenoses of over 50% luminal loss (CV% 8.7, ICC 0.97) but agreement on assessment of less severe lesions was poor (CV% 208.7, ICC 0.51). CONCLUSION: This study demonstrates that CABGs can be quantitatively evaluated using MSCT, and that significant lesions present in all CABG segments can be reliably identified. Agreement between MSCT and QCA for lesions of less than 50% luminal loss was poor.

Health related quality of life of patients with refractory angina before and one year after enrolment onto a refractory angina program.

OBJECTIVE: This study was designed to assess the impact of a refractory angina programme on the health related quality of life for patients with chronic refractory angina (CRA) one year following enrolment. DESIGN: A one year prospective audit. SETTING: Specialist refractory angina clinic at a tertiary cardiac referral centre. PATIENTS: 69 consecutive refractory angina patients referred to a regional refractory angina centre from 1/03/2001 to 1/09/2002. INTERVENTIONS: Pain treatment algorithm in accordance with the recommendations of the national refractory angina guideline committee. MAIN OUTCOME MEASURES: Improvements in quality of life indices were assessed using Seattle angina questionnaire (SAQ), and short form-12 (SF-12) with changes in mood determined using the hospital anxiety and depression (HAD) questionnaire. RESULTS: All dimensions of the SF-12 and SAQ were superior at one year with significant improvement seen with the mental component of SF-12 (p = 0.023), and four of the five SAQ domains, angina stability (p = 0.028), angina frequency (p=0.02), treatment satisfaction (p=0.001) and quality of life (p < 0.001). All the significant changes within the SAQ domains were large enough to be considered clinically relevant. At one year the anxiety and depression domains were significantly improved from baseline (p = 0.015, 0.018) with clinical anxiety levels falling significantly from 55% to 40%, a relative reduction of 28% (p = 0.008). CONCLUSIONS: Implementation of the national refractory angina guidelines in a prospective study of 69 consecutive CRA patients significantly improved health related quality of life status at one year.

Complex stenosis morphology predicts late reocclusion during follow-up after myocardial infarction in patients with patent infarct-related coronary arteries.

BACKGROUND: Whether angiographic morphology of infarct-related residual stenoses continues to affect prognosis after discharge is not known. METHODS: We studied 175 patients after their myocardial infarction who required nonurgent coronary angioplasty for residual myocardial ischemia. The findings at diagnostic coronary angiography were compared with those before angioplasty (mean of 7 months later). Infarct-related stenoses were classified as complex or smooth. Stenosis progression was defined as >0.5 mm diameter reduction. RESULTS: One hundred twenty-one (69%) infarct-related stenoses were complex. At restudy, total occlusion was found in 41 (35%) of the infarct-related complex stenoses compared with 7 (13%) smooth stenoses (P = .001). Reocclusion occurred in 16 (55%) of 29 complex infarct-related stenoses with thrombus, compared with 25 (28%) of 88 without thrombus (P = .01). During follow-up, 46 patients (26%) had cardiac events. Of these, 70% had complex lesions at study entry compared with 30% smooth (P < .05). CONCLUSIONS: Residual angiographically complex stenoses after an uncomplicated myocardial infarction are associated with a greater risk of reocclusion and may predispose to coronary events at follow-up.

Coronary stenosis progression differs in patients with stable angina pectoris with and without a previous history of unstable angina.

OBJECTIVES: To compare the evolution of stenoses responsible for acute coronary events with those not associated with acute coronary syndromes. METHODS AND RESULTS: We prospectively studied angiographic stenosis progression in 190 stable angina patients, with single vessel disease, who were awaiting non-urgent coronary angioplasty. Sixty four patients had a previous history of unstable angina (Group 1) and 126 patients had no history of unstable angina (Group 2). Culprit stenoses were classified as "complex' or "smooth'. At restudy, 8 +/- 4 months after the first angiogram, 12 of 63 culprit stenoses in Group 1 had progressed and seven of 125 in Group 2 (19% vs 6%, P = 0.0044). Thirteen of 68 complex culprit stenoses had progressed, compared with only 6 of 120 smooth culprit stenoses (19% vs 5%, P = 0.003). Coronary events occurred in 12 Group 1 patients and nine Group 2 patients (P = 0.02). CONCLUSIONS: In patients with stable angina, stenoses associated with previous episodes of unstable angina are more likely to progress than stenoses not associated with previous unstable angina. Unstable coronary atherosclerotic plaques, even those that have been clinically stable for more than 3 months, may retain the potential for rapid progression to total occlusion.

Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris.

OBJECTIVES: This study sought to compare the evolution of complex culprit stenoses in patients with stable and those with unstable angina pectoris. BACKGROUND: Complex coronary stenoses are associated with adverse clinical and angiographic outcomes. However, it is not known whether the evolution of complex stenoses differs in unstable angina versus stable angina pectoris. METHODS: We prospectively assessed stenosis progression in 95 patients with unstable angina whose angina stabilized with medical therapy (Group 1) and 200 patients presenting with stable angina (Group 2). After diagnostic angiography, all patients were placed on a waiting list for coronary angioplasty and restudied at 8 +/- 4 (mean +/- SD) months later. In each patient the presumed culprit stenosis was identified and classified as complex (irregular borders, overhanging edges or thrombus) or smooth (absence of complex features). Stenosis progression, as assessed by computerized angiography, was defined as > or = 20% diameter reduction or new total occlusion. RESULTS: At the first angiogram, 364 stenoses > or = 50% and 383 stenoses < 50% were identified. At restudy, 36 (15%) of 236 stenoses progressed in 29 Group 1 patients and 36 (7%) of 502 stenoses in 31 Group 2 patients (p = 0.001). Forty-five (88%) of 51 stenoses > or = 50% and 6 (29%) of 21 stenoses < 50% that progressed developed to total coronary occlusion (p = 0.001). More culprit stenoses progressed in Group 1 than in Group 2 (p = 0.006), whereas progression of nonculprit stenoses was not significantly different in both groups. Culprit complex stenoses progressed more frequently in Group 1 than in Group 2 (p = 0.01). During follow-up, 3 patients died (myocardial infarction), and 51 had a nonfatal coronary event. Culprit stenoses progressed in 15 (54%) of the 28 patients with a nonfatal coronary event in Group 1 and in 9 (39%) of 23 patients in Group 2 (p = NS). Complex morphology (p < 0.001) and unstable angina at initial presentation (p < 0.01) were predictive factors for progression of culprit stenoses. CONCLUSIONS: A larger proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.

The natural history of unheralded complex coronary plaques.

OBJECTIVES: This study sought to assess the behavior of unheralded complex lesions in patients with no previous history of acute coronary ischemia. BACKGROUND: Angiographically complex coronary stenoses appear to originate from plaque disruption and are associated with rapid progression early and late after acute coronary events. Complex lesions may occur without symptoms, but neither the incidence nor the behavior of these unheralded complex lesions is known. METHODS: We studied 222 patients with chronic stable angina who were on a waiting list for single-vessel percutaneous transluminal coronary angioplasty of an unoccluded lesion and underwent repeat angiography immediately before the procedure as part of routine practice or shortly after a coronary event. Patients with a previous episode of myocardial infarction or unstable angina were not included. Angiograms were analyzed quantitatively and qualitatively using established methods. A change of +/- 15% stenosis severity or total coronary occlusion defined categoric change. RESULTS: At first angiography, there were 52 unheralded complex target lesions (23%) and 170 smooth target stenoses (77%). Stenosis severity did not differ between complex and smooth target lesions at first and second angiography at a mean (+/- SD) interval of 7 +/- 4 months. At follow-up, seven complex lesions had progressed (14%) compared with six smooth lesions (4%, p < 0.02). Total occlusion developed in four complex lesions and one smooth lesion. Overall, complex stenoses progressed by 3 +/- 13% compared with 0.5 +/- 7% in the smooth stenoses (p = 0.15). Complex stenoses were 4.2 times more likely to progress than smooth stenoses (95% confidence interval 1.2 to 15.2 [Cornfields method]). Clinical events developed in seven patients. One complex lesion regressed and became smooth, and three smooth stenoses became complex at follow-up. CONCLUSIONS: Morphologically complex stenosis can develop without an episode of acute coronary ischemia and are relatively common in patients awaiting single-vessel angioplasty. Our study demonstrates that like their clinically heralded counterparts, these unheralded complex stenoses are at higher risk of progression than smooth stenoses.

Rapid angiographic progression of coronary artery disease in patients with angina pectoris. The role of complex stenosis morphology.

BACKGROUND: Rapid disease progression commonly underlies acute coronary events, and "complex" stenosis morphology may play a role in this phenomenon. METHODS AND RESULTS: We studied the role of complex stenosis morphology in rapid disease progression in 94 consecutive patients awaiting routine coronary angioplasty. Coronary arteriography was repeated at 8 +/- 3 months' follow-up, immediately preceding angioplasty (68 patients) or after an acute coronary event (26 patients). Disease progression of 217 stenoses, of which 79 (36%) were "complex" and 138 (64%) were "smooth," was assessed by computerized angiography. At presentation, 63 patients had stable angina pectoris and 31 had unstable angina that settled rapidly with medical therapy. At follow-up, 23 patients (24%) had progression of preexisting stenoses and 71 (76%) had no progression. Patients with progression were younger (55 +/- 12 years) than those without (58 +/- 9 years) but did not differ with regard to risk factors, previous myocardial infarction, or severity and extent of coronary disease. Twenty-three lesions (11%) progressed, 15 to total occlusion (11 complex and 4 smooth; 65%). Progression occurred in 17 of the 79 complex stenoses (22%) and in 6 of the 138 smooth lesions (4%) (P = .002). Mean stenosis diameter reduction was also significantly greater in complex than in smooth lesions (11.6% versus 3.9% change; P < .001). Acute coronary events occurred in 57% of patients with progression compared with 18% of those without progression (P < .001) and were more frequent in patients who presented with unstable angina (P = .002). CONCLUSIONS: Rapid stenosis progression is not uncommon, and complex stenoses are at risk more than smooth lesions.

Beta adrenoceptor density in the donor heart: a guide to prognosis?

BACKGROUND: Failure of the donor (graft) heart is the main cause of mortality in the first month after orthotopic cardiac transplantation. In a preliminary study marked downregulation of cardiac beta adrenoceptor density was found in apparently normal donor hearts of recipients who developed severe cardiac failure soon after implantation. Cardiac beta adrenoceptors are an important factor in the development of cardiac failure in the human heart. The aim of this study therefore was to determine whether fatal graft failure in the first month after transplantation is associated with downregulation of beta adrenoceptor density in the donor heart. PATIENTS AND METHODS: Right ventricular endomyocardial biopsy specimens were taken from consecutive adult donor patients immediately before implantation. A previously described radioligand binding method was used to determine beta adrenoceptor density in consecutive patients who developed fatal graft failure and died within 1 month of transplantation and in a group of control donors transplanted during the same period. RESULTS: Perioperative fatal graft failure developed in 13 patients. Forty one specimens from donor hearts that were transplanted into recipients who did not develop fatal graft heart failure formed the control group. There were no systematic differences in donor or recipient characteristics between the graft heart failure and control groups. In particular donor catecholamine requirement and recipient pulmonary vascular resistance did not differ between groups. Total beta adrenoceptor density was reduced in the fatal graft heart failure group compared with that in the controls (13.4 (7) fmol/mg v 21 (7) fmol/mg; P < 0.01). There was a positive correlation between beta adrenoceptor density in the donor heart and time to death in the graft heart failure group (r2 = 0.3, P < 0.05). The beta adrenoceptor binding affinity (Kd) did not differ between the graft failure group and the controls (47 (6) pM v 44 (7) pM). CONCLUSION: The development of perioperative fatal cardiac failure after orthotopic cardiac transplantation is associated with downregulation of beta adrenoceptors in the donor heart before implantation.

Angiographic stenosis progression and coronary events in patients with 'stabilized' unstable angina.

BACKGROUND: Recent studies suggest that angiographically complex coronary stenoses are associated with an adverse short-term outcome. It is not known, however, if this applies to unstable angina patients who stabilize on medical therapy. METHODS AND RESULTS: We prospectively studied 85 consecutive patients with unstable angina who stabilized on medical therapy but were found to require angioplasty for treatment of obstructive coronary disease. Angiography was carried out at admission, and patients were restudied 8 +/- 4 months (mean +/- SD) after the first angiogram. Ischemia-related stenoses were identified and classified as "complex" (irregular borders, overhanging edges, or thrombus) or "smooth" (absence of complex features). Stenosis progression (> or = 20% diameter reduction or new total occlusion) was assessed by automated edge detection. At initial angiography, there were 198 stenoses (> or = 50%, 102), of which 85 (54 complex and 31 smooth) were ischemia related. At restudy, 21 ischemia-related stenoses and 8 non-ischemia-related stenoses progressed (25% versus 7%, P = .001). Seventeen of the 21 ischemia-related stenoses that progressed developed into total occlusion compared with 3 of the 8 non-ischemia-related stenoses (P = .02). Changes in average stenosis severity and in absolute stenosis diameter were significantly larger in ischemia-related stenoses than in non-ischemia-related stenoses (P = .03). Eighteen (34%) complex stenoses progressed, compared with 3 (10%) smooth lesions (P = .02). During follow-up, 1 patient died (myocardial infarction) and 25 patients had nonfatal coronary events that were associated with progression of ischemia-related stenoses in 14 (56%). CONCLUSIONS: In unstable angina patients who stabilize medically, subsequent short-term stenosis progression and coronary events are common. The unstable coronary lesion (particularly complex stenoses) is often not stabilized and will continue to progress over the ensuing months.

Differential progression of complex and smooth stenoses within the same coronary tree in men with stable coronary artery disease.

OBJECTIVES: We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease. BACKGROUND: Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient. METHODS: We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions > or = 10 mm long, at a major branching point or with > 85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers. RESULTS: All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by > or = 15% was seen in only eight complex stenosis (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean +/- 1 SD 5.8 +/- 13% vs. -0.06 +/- 6%, p < 0.01). On average, the annual rate of growth was 11.4 +/- 28% and 1.5 +/- 14% for complex and smooth lesions, respectively (p < 0.01). CONCLUSIONS: Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease.

Cardiac chamber-specific beta-adrenoceptor regulation and sympathetic innervation.

We assessed by radioligand binding techniques the effect of cardiac failure on beta-adrenoceptor density in 5 hearts from patients undergoing repeat transplantation and 5 normal (unused donor) hearts. Right ventricular total and subtype beta-adrenoceptors in the denervated repeat-transplant hearts were down-regulated compared with the normally innervated controls. Within the denervated hearts, beta 1-adrenoceptors were selectively down-regulated in the right ventricle compared with the left ventricle. Tissue noradrenaline content confirmed sympathetic denervation in the transplanted hearts. Thus, regional sympathetic innervation is not necessary for chamber-specific beta-adrenoceptor down-regulation; other mechanisms for this process should be sought.

Creatine kinase MB isoforms: sensitive markers of ischemic myocardial damage.

We investigated the use of creatine kinase (CK) MB isoforms as a marker of myocardial cell injury in a preliminary study of 16 patients with chronic stable angina after successful percutaneous transluminal coronary angioplasty (PTCA) and 25 patients after coronary artery bypass grafting (CABG). Three control groups were studied: apparently healthy volunteers (n = 31), patients undergoing thoracotomy (n = 10), and patients undergoing routine coronary angiography (n = 9). Patients in the PTCA group showed an association between ischemic ST segment changes lasting > 3 min and a transient increase in the MB2/MB1 ratio; however, all had total CK-MB activity within normal limits. Routine coronary angiography subjects had no significant change in MB2/MB1. In the CABG patients, MB2/MB1 peaked within 1 h after the cross-clamp release and returned to baseline by 24 h postoperatively. The median time to peak MM3/MM1 and total CK-MB activity was 2 and 8 h after reperfusion, respectively, returning to baseline values by 2 and 5 days, respectively. After thoracotomy, MB2/MB1 was increased only in elderly patients (n = 5) with risk factors for ischemic heart disease; total CK-MB activity was increased in only three of these. Apparently, CK-MB isoforms can detect myocardial damage in clinical settings with less overt damage than myocardial infarction.

The effect of orthotopic transplantation on total, beta 1- and beta 2-adrenoceptors in the human heart.

1. [125I]-(-)pindolol binding was used to determine beta-adrenoceptor density in homogenate preparations of right ventricular endomyocardial biopsies from 43 non-rejecting patients over the first 13 months following cardiac transplantation. The selective beta 1 subtype antagonist ligand CGP 20712A was used to determine the subtype density in 32 of the patients. Biopsy specimens from 15 donor hearts were used as controls. 2. beta-adrenoceptor density (expressed in terms of fmol mg-1 protein) was increased in the group of transplanted hearts as a whole compared with the donor hearts with respect to total (35 +/- 2 vs 23 +/- 2) and the beta 1 subtype (25 +/- 2 vs 16 +/- 2) whereas the beta 2 subtype and radioligand dissociation constant did not differ. 3. Non-parametric analysis of variance of total receptor density over time revealed significant heterogeneity which appears to be due to a discrete increase in beta-adrenoceptor density during the 4th post operative month. 4. These results indicate that beta-adrenoceptor density is not constant following transplantation. Furthermore, the increase in receptor density following transplantation is due mainly to an increase in the beta 1 subtype without a significant change in the beta 2 subtype.

Sedation for fibreoptic bronchoscopy: comparison of alfentanil with papaveretum and diazepam.

Sedation for fibreoptic bronchoscopy should produce optimal conditions for the operator, patient comfort and rapid recovery allowing early discharge home. We have compared a regimen producing 'light' sedation with a more traditional regimen producing 'deep' sedation. Seventy-six patients undergoing fibreoptic bronchoscopy under topical anaesthesia were randomized to receive either light sedation with the short acting opiate, alfentanil (median dose 1.1 mg, range 0.5-2.6 mg) or deep sedation with a combination of papaveretum (median dose 10 mg, range 5-15 mg) and diazepam (median dose 8 mg, range 0-20 mg). Both techniques gave equally good operating conditions, although patients given alfentanil coughed less than those given papaveretum and diazepam (U = 2.814 P less than 0.01). Patients recorded their degree of apprehension on a visual analogue scale prior to sedation and the actual degree of comfort experienced after recovery. There was no significant difference between apprehension or comfort between the groups. This was despite a higher degree of amnesia for an irrelevant object shown during the bronchoscopy in the deeply sedated group (chi 2 = 21.084 P less than 0.001). Patients given alfentanil performed significantly better in a modified Romberg test (chi 2 = 4.357 P less than 0.05) and a visualisation test (t = 3.035 P less than 0.01) two hours after the bronchoscopy. Alfentanil produced good operating conditions, patient comfort, less cough and a more rapid recovery, compared to the deep sedation regimen, and is an ideal sedative for fibreoptic bronchoscopy.