Gatekeeper for coronary angiography: reply

We thank Geluk and Zijlstra for their kind words as well astheir considerations and proposals. The latter hits right intothe heart of the issue: should one stick to the ‘anatomic’paradigm urging us to detect and treat coronary stenoses andcalcifications rather than follow     

Effects of ketanserin on epicardial coronary arteries after coronary angioplasty in patients with stable angina

Previous studies have demonstrated the development of vasoconstrictionimmediately after percutanous coronary angioplasty (PTCA), distalto the dilated stenosis, presumably resulting from endothelialinjury. We have investigated the role of 5-HT₂ receptors inmediating vasomotor changes in proximal and distal coronarysegments and coronary stenoses, immediately after successfulPTCA in patients with chronic stable angina. We compared theeffects of the intracoronary infusion of 1 mg ketanserin (5-HT₂receptor antagonist) on proximal and distal coronary arterialsegments immediately after PTCA in both vessels subjected toPTCA and control vessels. Coronary diameters, before and afterangioplasty and after ketanserin administration, of proximaland distal segments and coronary stenoses were measured by computerizedquantitative coronary angiography (CAAS system) in 12 patients(10 male, two female; mean age 54 ±6 years) with stableangina subjected to PTCA. After coronary angioplasty, vasoconstrictionwas observed in the segment distal to the dilated stenosis butnot in the distal segments of control vessels ( – 0.12± 0.04 and – 0.02 ± 0.02 mm respectively,P<0.05). After ketanserin infusion significant dilatationwas found in the distal segments of both PTCA vessels and controlvessels, but the dilatation was greater in the PTCA vessels(P<0.05). No significant changes were found in the proximalsegments of either PTCA or control vessels, or at the PTCA site.In conclusion, the vasoconstriction distal to the site of PTCAis mediated, at least in part, via 5-HT₂ receptors.     

Response of high-sensitivity C-reactive protein to percutaneous coronary intervention in patients with acute coronary syndrome

Percutaneous coronary intervention (PCI) provokes an inflammatory reaction, as shown by increased concentrations of plasma C-reactive protein (CRP) after PCI. However, the changes of CRP levels after PCI in patients with acute coronary syndrome (ACS) have not been well evaluated. We evaluated the characteristics of the patients with elevated CRP response after PCI and whether an increase in CRP after PCI predicts long-term prognosis in patients with ACS. We studied consecutive 360 patients with ACS who underwent elective coronary stenting. Inflammatory response to PCI was calculated as the difference between the peak postprocedural hsCRP level and the preprocedural hsCRP level (ΔCRP). Twelve months follow-up data were obtained and clinical outcomes were compared with ΔCRP. In receiver operating characteristics analyses, the cutoff point of ΔCRP for major adverse cardiac events (MACE) was 3.0 mg/l, which yielded sensitivity of 61.7% and specificity of 69.7%. The patients with ΔCRP > 3 mg/l revealed higher incidence of myocardial infarction (37.7 vs 14.6%, P < 0.001), and ACC/AHA type B2/C lesion (81.5 vs 68.7%, P = 0.006) than in patients with low ΔCRP. White blood cell count, low-density lipoprotein cholesterol, peak creatinine kinase-MB, and peak troponin T were significantly elevated in patients with ΔCRP > 3 mg/l than in those with ≤3 mg/l. There was significant correlation between ΔCRP and the changes in troponin T after PCI (r = 0.210, P < 0.001). An increase in hsCRP > 3 mg/l after PCI had a higher predictive value for the occurrence of MACE than low hsCRP elevation (hazard ratio 2.1, P = 0.005). In multivariate analysis, ΔCRP and peak troponin T were independent predictors of MACE (P < 0.001 and P = 0.013, respectively). In conclusion, postprocedural hsCRP elevation >3 mg/l was associated with higher incidence of MACE in patients with ACS. ΔCRP determinations may be of value for risk stratification after PCI.     

Concurrent coronary and carotid artery surgery: an open debate: reply

We read with interest the letter from Barili et al. onour work ‘Concurrent coronary artery surgery: factorsinfluencing perioperative outcome and long-term results’.¹We thank Barili et al. for their comments that need ourreply. First, we share their doubts regarding the precise impact ofasymptomatic carotid artery stenosis     

Distribution of coronary atherosclerosis in patients with coronary artery disease

The distribution of coronary atherosclerosis has not been fully clarified. We measured coronary artery calcium score (CACS) in 624 consecutive patients for the right coronary artery (RCA), left main trunk (LMT), left anterior descending coronary artery (LAD), and left circumflex coronary artery (LCx), then calculated total CACS. Coronary artery calcium score was measured using the Agatston method. We divided these patients into four groups: CACS 1–100 (Group A, n = 267), CACS 101–400 (Group B, n = 160), CACS 401–1000 (Group C, n = 110), and CACS >1000 (Group D, n = 87). In Group A, B, and C, the CACS in LAD was significantly higher than in the other three arteries (P < 0.0001). In Group D, the CACS was not significantly different between LAD and RCA (P = 0.6930). In Groups A, B, and C, coronary artery calcium (CAC) was more frequently found in LAD compared with other arteries (P < 0.0001). However, in Group D the prevalence of CAC was not significantly different among the three arteries (P = 0.4435). Coronary artery calcium was found more frequently in LAD than in the other coronary arteries in patients with mild to high CAC, but not in those with very high CAC.     

Restenosis after coronary angioplasty for rapidly progressive coronary stenosis

OBJECTIVES: We hypothesized that percutaneous transluminal coronary angioplastyperformed on coronary stenoses that have demonstrated rapidangiographic progression would be associated with a high riskof restenosis. BACKGROUND: High rates of restenosis have been documented after percutaneoustransluminal coronary angioplasty of unstable lesions and oflesions that recurrapidly after a successful initial angioplasty.This suggests that the ‘activity’ of the plaqueat the time of angioplasty may be an important factor determiningthe risk of restenosis. METHODS: In our institution we recommend angiographic follow-up for allpatients with successful percutaneous transluminal coronaryangioplasty. In this way we identified 86 consecutive patientswho, at the time of angiographic follow-up had not developedrestenosis at the dilated site, butrequired a further percutaneoustransluminal coronary angioplasty at a different site (whichwas successful). Based on quantitative angiographic measurements,45 of these lesions (rapidly progressive lesions) had significantlyincreased in severity in the interval between the two angiograms(7.7 ± 3.3 months) while 41 (stable lesions) had not.Rapid progression was defined as a >0.4 mm decrease in minimallumen diameter between initial angiography and percutaneoustransluminal coronary angioplasty. All 86 patients had furtherangiographic follow-up 6 months later. RESULTS: Baseline clinical and angiographic variables were similar inboth groups except that a higher proportion of patients in therapid progression group had unstable angina (20% vs 5% P<0.05).Late loss during follow-up did not differ statistically betweengroups (0.31 mm) and minimal lumen diameter at follow-up wasalso similar (stable lesion group=1.40 ± 0.48 mm; rapidlyprogressive lesion group=1.30 ± 0.59 mm). The loss index(late loss divided by acute gain) was also similar in both groups(0.45 ± 0.52 in the stable lesion group, 0.37 ±0.76 in the rapidly progressive lesion group). A strong correlationbetween acute gain and late loss was observed in the stablelesion group (r=0.61; P<0.0001); by contrast, there was norelationship between these two variables in the rapidly progressivelesion group (r=0.20; P=0.19). CONCLUSIONS: Percutaneous transluminal coronary angioplasty in patients withunstable angina or with early recurrence after a first percutaneoustransluminal coronary angioplasty is associated with anincreasedrisk of restenosis. By contrast, this study shows that angiographicinstability, as evidenced by rapid stenosis progression, hasno deleterious effect on the occurrence of restenosis. Percutaneoustransluminal coronary angioplasty thus appears as a reasonabletherapeutic option for coronary stenoses that have demonstratedrapid angiographic progression in the months prior to the procedure.     

Are acute coronary syndromes risk models too complex? reply

We thank Drs Gale and Manda for their interest in our study.¹We believe it is important to explore why validated risk scoresare often not applied in the ‘real world’, and concurthat their perceived complexity may constitute the greatestbarrier to more widespread use. However,     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3·5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4·7 ± 0·5 vs 4·6± 0·6 for the left anterior descending, 4·6± 0·4 vs 4·6 ± 0·3 for theleft circumflex and 4· ± 0·4 vs 4·4± 0·5 for the right coronary artery (all P=non-significant).The subsets of mitral valve prolapse patients with differentclinical ‘ischaemic’ manifestations were similarin terms of the calculated coronary flow reserve in all threemajor epicardial coronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Significant coronary restenosis limits the recovery of regional left myocardial dysfunction achieved after successful coronary angioplasty

Impaired regional left ventricular function has been shown toimprove after successful transluminal coronary angioplasty,but there are no data concerning the effect of coronary restenosison this recovery. Therefore, the short- (1 month) and midterm(5.5 months) evolution of systolic regional left ventricularfunction was prospectively investigated in 41 patients undergoingsuccessful coronary angioplasty. In patients with resting hypokineticareas before angioplasty and no restenosis (n=8), regional functionimproved from –6.0±2.9 to –2.9±2.4SD/segment (P<0.01) in the short-term, without further significantchanges at mid-term. Patients with hypokinetic areas and coronaryrestenosis 70% (n = 15) also showed early functional recoveryfrom –5.1 ± 2.2 to –1.4 ± 2.5 SD/segment(P <0.0001) but, in contrast with the other subset of patients,a significant reduction to –3.9±2.3 SD/segment(P<0.0001) was observed at mid-term. In spite of this, regionalfunction was still better than before angioplasty (P <0.01).No significant changes were observed in patients without eitherasynergy or restenosis (n = 16). The small number of cases withoutpreliminary hypokinesis and development of restenosis 70% (n= 2) precluded an analysis of this situation, but a new andsevere hypokinetic defect was recognized in one patient in alater study. We conclude that the improvement in regional myocardialfunction observed early after successful dilation of the culpritvessel is partially lost when significant restenosis develops.     

Statins and percutaneous coronary intervention.

We have read with interest the article by Briguori et al.¹and we have several comments for the authors. The paper is arandomized study on pre-treatment with statins before percutaneousintervention, showing reduction of post-procedural myocardial     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3.5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4.7 ± 0.5 vs 4.6 ± 0.6 for theleft anterior descending, 4.6 ± 0.4 vs 4.6 ± 0.3for the left circumflex and 4. ± 0.4 vs 4.4 ±0.5 for the right coronary artery (all P=non-significant). Thesubsets of mitral valve prolapse patients with different clinical‘ischaemic’ manifestations were similar in termsof the calculated coronary flow reserve in all three major epicardialcoronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Insulin resistance and coronary artery disease

Summary The purpose of the present study was to quantitate insulin-mediated glucose disposal in normal glucose tolerant patients with angiographically documented coronary artery disease (CAD) and to define the pathways responsible for the insulin resistance. We studied 13 healthy, normal weight, normotensive subjects with angiographically documented CAD and 10 age-, weight-matched control subjects with an oral glucose tolerance test and a 2-h euglycaemic insulin (40 mU · m⁻²· min⁻¹) clamp with tritiated glucose and indirect calorimetry. Lean body mass was measured with tritiated water. All CAD and control subjects had a normal oral glucose tolerance test. Fasting plasma insulin concentration (66 ± 6 vs 42 ± 6 pmol/l, p < 0.05) and area under the plasma insulin curve following glucose ingestion (498 ± 54 vs 348 ± 42 pmol · l⁻¹· min⁻¹, p < 0.001) were increased in CAD vs control subjects. Insulin-mediated whole body glucose disposal (27.8 ± 3.9 vs 38.3 ± 4.4 μmol · kg fat free mass (FFM)⁻¹· min⁻¹, p < 0.01) was significantly decreased in CAD subjects and this was entirely due to diminished non-oxidative glucose disposal (8.9 ± 2.8 vs 20.0 ± 3.3 μmol · kg FFM⁻¹· min⁻¹, p < 0.001). The magnitude of insulin resistance was positively correlated with the severity of CAD (r = 0.480, p < 0.05). In the CAD subjects basal and insulin-mediated rates of glucose and lipid oxidation were normal and insulin caused a normal suppression of hepatic glucose production. In conclusion, subjects with angiographically documented CAD are characterized by moderate-severe insulin resistance and hyperinsulinaemia and should be included in the metabolic and cardiovascular cluster of disorders that comprise the insulin resistance syndrome or ’syndrome X'. [Diabetologia (1996) 39: 1345–1350] Received: 6 February 1996 and in revised form: 29 May 1996     

Intravascular ultrasound assessment of coronary artery involvement in Fabry disease

Summary Aim  We used intravascular ultrasound (IVUS) to characterize coronary artery involvement in patients with Fabry disease (FD). Methods  Nine FD patients (5 women) were matched to 10 control patients (5 women) chosen from our IVUS database. Standard volumetric IVUS analyses were performed along with assessment of plaque echodensity. Results  Plaques in FD patients were diffuse and hypoechogenic compared with more focal and more echogenic lesions in control patients. Echogenicity of plaques was significantly lower in FD patients (median 30.7  ±  12.9 vs 55.9  ±  15.7, p  =  0.0052, mean 37.2  ±  15.6 vs 66.2  ±  13.3, p  =  0.0014). Diffusiveness was assessed as differences between mean and median plaque burden versus the plaque burden in each of the analysed cross-sections. These differences were lower in FD vs controls (5.8  ±  4.8 vs 8.7  ±  6.6, p  <  0.001 for mean, and 5.8  ±  4.9 vs 8.8  ±  7.3, p  <  0.001 for median) indicating a more diffuse involvement. The occurrence of lipid cores was significantly higher in FD patients than in controls (2.4  ±  1.5 vs 1.0  ±  0.94, p  =  0.02). Conclusion  IVUS showed diffuse hypoechogenic plaques in patients with FD. The explanation may be higher lipid content in plaques and accumulation of glycosphingolipid in smooth-muscle and endothelial cells. Competing interests: None declared References to electronic databases: Fabry disease: OMIM +301500.     

Influence of nifedipine on coronary haemodynamics and myocardial metabolism in coronary artery disease

The effect of 30 mg sublingual nifedipine on cardiac metabolismand haemodynamics was studied during two identical periods ofpacing in 11 patients with chronic coronary artery disease.The pace time to angina pectoris improved after nifedipine in6 patients, deteriorated in 2 and was unchanged in 3. Nifedipinedecreased blood pressure (12%), rate pressure product (10%)and coronary vascular resistance (17%) during pacing. Aorto-coronarysinus (A-Cs) oxygen difference decreased at rest (9%) and postpacing(10%) after nifedipine, although an opposite tendency in coronarysinus blood flow resulted in unchanged myocardial oxygen uptakethroughout the study. Although mean myocardial lactate extractionafter nifedipine was unchanged during pacing in the whole groupof patients, it increased in 9 patients who showed a net lactaterelease at control pacing (from –50.9±33.5% to–35.9±30.2%, P>0.05). Nifedipine increased freefatty acid (FFA) extraction during pacing (from 1.5±12.9%to 17.4±13.1%, P<0.02) and uptake (from 1.8±8.5to 11.1±10.6 µmol min^–1, P<0.05). Nifedipineinfluenced only glucose exchange significantly (46% decreasedextraction) at 5 min postpacing. The A–Cs citrate gradientlessened 30–40% postpacing after nifedipine administration. Since the unloading effects of nifedipine did not alter myocardialoxygen uptake, the most important net haemodynamicfinding wasthe decrease in coronary vascular resistance. Although no significantantianginal effect of a fixed dose of nifedipine was found,the increased uptake of FFA may reflect improved myocardialoxidative metabolism after nifedipine     

Mechanisms of adenosine-induced epicardial coronary artery dilatation

BACKGROUND: In order to ascertain whether human adenosine-induced dilatationof epicardial arteries is direct or flow-mediated, we comparedthe effects of intracoronary adenosine infusion on epicardialcoronary arteries with those produced by dypiridamole, a selectivearteriolar vasodilator. METHODS AND RESULTS: In 24 patients with angiographically normal coronary arteries,coronary blood flow velocity was measured by a Doppler wireduring intracoronary infusion of adenosine or dipyridamole,which is known to increase intramyocardial adenosine concentration.Coronary angiograms were obtained at baseline and immediatelyafter the end of each infusion period; coronary diameters 5mm distal to the wire tip were measured by computer-assistedquantitative coronary angiography. Peak coronary blood flowvelocities during adenosine or dipyridamole infusions were similar(52·0 ± 15·5 and 47·9 ± 24·2cm. s^–1, P=ns). Coronary diameters immediately after adenosineand dipyridamole infusions were similar and both higher thanthat at baseline (2·80 ± 0·63 and 2·80± 0·64 vs 2·44 ± 0·69 mm,P<0·05). The absolute and percentage increases ofcoronary artery diameters in response to adenosine were highlycorrelated to coronary blood flow velocity (R=0·622,intercept –0·10 ± 0·14, P=0·002and R=0·617 intercept –15·2 ± 9·9,P=0·001, respectively); similar correlations were foundin response to dipyridamole (R=0·708, intercept –0·44± 0·19, P<0·001 and R=0·649,intercept –13·5 ± 8·7, P<0·001,respectively). Finally the absolute and percentage changes ofcoronary artery diameters caused by adenosine were highly correlatedto those caused by dipyridamole (R=0·840, P<0·001and R=0·836, P<0·001 respectively). CONCLUSIONS: A significant correlation exists between epicardial coronaryvasodilation and coronary blood flow velocity during intracoronaryadenosine infusion, thus suggesting that epicardial coronaryvasodilation induced by adenosine is predominantly flow-mediatedrather than direct. This conclusion is supported by the observationthat similar findings were obtained using dipyridamole, whichcan only dilate epicardial coronary arteries indirectly, throughthe increase in coronary blood flow velocity caused by the inhibitionof intramyocardial adenosine re-uptake.     

Increased cardiac sympathetic nervous activity in patients with unstable coronary heart disease

We have evaluated overall and cardiac sympathetic activity in47 patients undergoing coronary angiography, 27 with stableangina of at least 3 months duration, and 20 with unstable ischaemicsymptoms within this period. Cardiac and overall sympatheticactivity were assessed using radiotracer noradrenaline kinetictechniques to measure cardiac and total noradrenaline spilloverto plasma. Overall sympathetic activity (whole body noradrenaline spillover)was similar in the two groups, whereas cardiac sympathetic activity(cardiac noradrenaline spillover) was strikingly increased inthe patients with unstable ischaemic symptoms (102 ±23 pmol . min^–1 vs 34 ± 4 pmol . min^–1, P< 0.001), as was the cardiac to whole body noradrenalinespillover ratio (0.043 ± 0.008 vs 0.021± 0.005,P < 0.01). Coronary sinus bloodflow (50 ± 4 ml . min^–1vs 38 ± 4 ml . min^–1 P < 0.05) and coronarysinus noradrenaline concentration (2.60±0.38 nmol . 1^–1vs 1.41±0.17 nmol . 1^–1, P<0.01) were also increasedin the patients with unstable ischaemic syndromes. Left ventricularejection fraction was similar in the two groups (63 ±2% vs 62 ± 2%). Patients with unstable ischaemic symptoms within the previousthree months have increased cardiac sympathetic nervous activitycompared to patients with stable angina. This may in part explainwhy patients with unstable ischaemic syndromes are at increasedrisk of sudden cardiac death.     

Quantitative evaluation of coronary stenosis by coronary magnetic resonance angiography

Coronary magnetic resonance angiography (coronary MRA) can detect, noninvasively, a high proportion of severe stenotic lesions found on coronary angiograms. However, quantitative evaluation of coronary artery stenosis by coronary MRA has been performed only in a small number of patients. This study was designed to determine whether coronary MRA can assess the degree of stenosis using the two-dimensional segmented turbo-FLASH method (2D method). We studied 108 patients with technically adequate coronary MRA images. The blood flow signal intensity on coronary MRA was classified as markedly decreased, moderately decreased, or normal. The severity of coronary artery stenosis was determined by the caliper method, and coronary stenosis was rated using a seven-point scale (0%, 25%, 50%, 75%, 90%, 99%, and 100%) in accordance with the American Heart Association classification system. Patients were classified into three groups: normal coronary artery (0%–25% stenosis), moderate stenosis (50%–75% stenosis), and severe stenosis (90%–100% stenosis). The degree of stenosis on coronary angiography and the decrease in coronary MRA signal intensity were compared. The right coronary artery was evaluated in 64 patients and the left coronary artery in 73 patients. When a marked or moderate decrease in coronary MRA blood flow signal intensity was defined as indicating stenosis, the sensitivity and specificity of coronary MRA for detecting angiographically severe stenosis were 85% and 80%, respectively. A moderate decrease in coronary MRA blood flow signal intensity detected angiographically moderate stenoses with a sensitivity of 38% and a specificity of 83%. Coronary MRA can detect a high proportion of severe stenoses but only a low proportion of moderate stenoses. Technical improvements are required before coronary MRA can be used clinically. Received: June 23, 2000 / Accepted: December 16, 2000     

The optimal mode of coronary revascularization for diabetics: A risk-adjusted long-term study comparing coronary angioplasty and coronary bypass surgery

Aims Some recent studies have reported superior outcomes for diabeticpatients following coronary bypass surgery compared with coronaryangioplasty. However, the available data are conflicting, arebased on relatively small numbers of diabetic patients, andhave limited duration of follow-up. The aims of this study wereto compare risk adjusted long- term survival in diabetic patientsfollowing first-time revascularization via either coronary bypasssurgery or coronary angioplasty; and, to identify variablesindependently associated with mortality. Methods and Results This was a two centre database project involving 15809 patientsundergoing either coronary angioplasty or coronary bypass surgeryas their initial revascularization procedure. Diabetes was presentin 1938 (12%). Mean follow-up was 4·6±2·7years for angioplasty and 6·6±4·3 yearssurgery diabetic patients. Multivariable time-related analysesin the hazard function domain for death were performed. Overallten-year survival for pharmacologically treated diabetics wasbetter after coronary bypass surgery (60%) than angioplasty(46%, <0·0001). However, the risk-adjusted survivaladvantage conferred by bypass surgery over angioplasty was strongestfor patients receiving oral agents for diabetic control (75%vs 62%) and less impressive for diet (84% vs 81%) and insulin-treateddiabetics (63% vs 64%). The major factors independently associatedwith worse outcome after angioplasty were incomplete revascularization,and the use of a sulfonylurea agent. The use of the left internalmammary graft improved survival in surgical patients. Conclusions In general, diabetic patients had better long-term survivalafter bypass surgery than angioplasty. Incomplete revascularizationand sulfonylurea therapy worsened outcome after angioplasty,and use of the left internal mammary improved outcome afterbypass surgery.The European Society of Cardiology     

Dilated cardiomyopathy and coronary flow reserve.

We read with interest the article by Rigo et al.¹ aboutthe prognostic impact of coronary flow reserve (CFR) by Dopplerechocardiography in dilated cardiomyopathy. The authors concludethat in patients with idiopathic dilated cardiomyopathy, theprognostic role of impaired microvascular CFR has been shownto be unfavourable. In our opinion, some points of     

The systemic and coronary haemodynamic effects of felodipine in patients with coronary heart disease

The cardiovascular effects of felodipine, a new arteriolar vasodilator,were studied in 22 patients with coronary heart disease. Therewere significant falls in blood pressure and systemic vascularresistance of 16 and 38% respectively (P = 0.001), thus affectingafter-load. Cardiac index and stroke index increased by 35 and12% respectively. There was reflex tachycardia-from 75 ±3to 85 ±3 b.p.m. (P =0.005). Coronary sinus blood /lowincreased from 134±9 to 191 ±17 ml/min (P<0.005)and myocardial arterio- venous oxygen difference narrowed from12.l±0.5 to 9.0±0.4 vols% (P<0.001) indicatingless oxygen usage. With the heart rate held constant by atrialpacing, cardiac index and stroke index increased by 30 and 26%(P<0.001), whilst systolic blood pressure and systemic vascularresistance fell by 20 and 29% (P<0.001). This would suggestthat the improved haemodynamics were largely secondary to after-loadreduction.