Long-term outcome of coronary angioplasty in elderly patients with post-infarction angina

The long-term clinical and angiographic outcome of 76 elderly(65 years) patients undergoing coronary angioplasty (PTCA) (83lesions attempted) for post-infarction angina (PIA) (group I)was compared with that of 83 elderly patients undergoing PTCA(105 lesions) for stable angina (group II). Age (70 ±4 years), gender (70% male) and major demographic variableswere similar in both groups. The mean left ventricular ejectionfraction was 56 ± 14% in group I vs 67 ± 14% ingroup II (P<0·01). In group I, PTCA was performedmore frequently for lesions located in the right coronary artery(35% vs 18%, P<0·01) and less frequently in the leftcircumflex artery (12% vs 26%, P<0·05). Although thepercentage of lesions with thrombi was higher in group I (16%vs 2%, P<0·0O1), the rate of angiographic successwas similar in both groups: 94% (78/83 lesions) in group I vs93% (98/105) in group II (ns). PTCA was successful in 67 patients(88%) in group I and in 74 (89%) in group II (ns). The rateof major complications was also similar in both groups (4%).Restenosis occurred in 36% vs 31% of the lesions in groups Iand II respectively (mean time to angiographic follow-up 7 ±2months) (proportion of cases with a repeat angiography: 79%ingroup I and 72% in group II). Restenosis was asymptomatic in57% vs 50% of the patients respectively. Actuarial event-freesurvival (freedom from death, acute myocardial infarction, coronarysurgery, or repeat angioplasty) after successful PTCA (meanfollow-up 22 ± 17 months) was 93%, 84%, 71%, and 54%at 1, 2, 3, and 4 years respectively in group I versus 90%,80%, 74%, and 56% in group II patients (ns). At last follow-up,92% vs 93% of our patients were still alive, and 85% vs 75%were asymptomatic (ns). In conclusion, the clinical indication(PIA versus stable angina) does not seem to affect the shortterm results of PTCA in elderly patients. Moreover, after asuccessful PTCA, elderly patients with PIA appear to have asa good mid-term outcome as those undergoing PTCA for stableangina.     

Prognostic significance of silent myocardial ischaemia during maximal exercise testing after a first acute myocardial infarction

Clinical, exercise, and angiographic variables, and long-termfollow-up were compared in patients, who, during maximal Bruceexercise testing after a first acute myocardial infarction (AMI),had positive responses to exercise testing (n = 116, 38% of303) with (n % 23, group I) or without (n = 93, group II) angina.Group I patients more often (52 vs 19%, P < 0.001) had ahistory of pre-infarction angina. Group II had a greater proportion(75 vs 52%, P < 0.05) of inferior wall AMI, whereas groupI had a greater proportion (30 vs 19%, P < 0.01) of non-Qwave AMI. Total exercise duration was significantly (P <0.01) longer in group II (7.6 ± 3.2 vs 5.5 ± 3.1min). Maximal exercise heart rate (144 ± 22 vs 133 ±21, beats . min^–1 P < 0.05 was also higher in groupII. A greater proportion of group II patients (37 vs 9%, P <0.05) had single-vessel disease, whereas multivessel diseasewas more common (91 vs 63% P < 0.03) in group I. Left ventricularfunction was similar in both groups. During follow-up (48 ±22 months) the incidence of cardiac death (group I, 3.3%, groupII, 4.8%), of recurrent infarction (group I, 4.8%, group II3.3%), and of revascularization procedures (group I, 28.5%,group II, 19.8%) were similar in both groups. Although asymptomaticexercise-induced ischaemia was associated with better exerciseperformance and less extensive coronary disease than symptomaticischaemia, it had the same long-term prognostic implications.     

Further elevation of the ST segment during the first hour of thrombolysis: A possible early marker of reperfusion

OBJECTIVES: To evaluate the clinical implications of early electrocardiographicchanges during thrombolysis in a randomized study in patientswith an acute myocardial infarction. BACKGROUND: Re-elevation of a rapidly resolving ST segment during thrombolysisis currently interpreted as a sign of re-occlusion, but a furtherelevation at very early stages of lytic therapy may not necessarilyhave the same implications. METHODS: In 214 patients with a first transmural acute myocardial infarctionof 4 h randomized to fibrinolytic (streptokinase group, n: 110)vs non fibrinolytic medical therapy (control group, n: 104),a standard 12 lead ECG was continuously recorded during thefirst 60 min and at 2, 4, 10, 16 and 24 h. Serial enzymes weremeasured during 72 h, and in 156 patients (73%) a coronary angiogramwas performed at 10–15 days. RESULTS: Within the first 20–40 min there was an additional STsegment elevation in 50 patients (45%) from the streptokinasegroup and in 19 from control group (18%) (P<0.0001) but theincrement was greater in the streptokinase group (1.2 ±1.4 vs 0.3 ± 1.4 mm, P<0.0001). In the streptokinasegroup, the interval from onset of pain to peak creatine kinaseMB was shorter in patients with additional ST segment elevationthan in those without it (699 ± 193 vs 856 ± 299min, P<0.01). Moreover, in-hospital mortality tended to belower in patients whose ST segment was elevated than in thosewithout such elevation (2150, 4%, vs 6160, 10%). Incidence ofrecanalization was high but comparable in these two subsets.In recanalized patients, with or without additional ST segmentelevation, the ST segment declined significantly at 1 h (–1.0 ± 1.7, P<0.001, vs 0.1 ± 1.5 mm, ns). CONCLUSIONS: Additional ST segment elevation is frequently observed duringthe first hour of intravenous thrombolysis with streptokinase.Its association with a subsequent early decline of ST elevation,reduced mortality, a shorter time interval to peak creatinekinase, and a high rate of late recanalization, suggest thatin some patients it is one of the earliest markers of reperfusion.     

Ventricular performance and prognosis after primary ventricular fibrillation complicating acute myocardial infarction

To examine the relationship between early arrhythmias, infarctsize and prognosis, we compared 22 consecutive patients survivingacute myocardial infarction (AMI) and primary ventricular fibrillation(VF) with a control population after AMI uncomplicated by primaryVF. Left ventricular ejection fraction (EF) was measured byradionuclide ventriculography before discharge from hospital.Mean EF was significantly reduced below normal following AMIwith or without primary VF (normal 0.57±0.05, mean±SD;P<0.01). Mean EF was lower among patients who survived primaryVF than among those with infarction uncomplicated by primaryarrhythmia (0.33 ±0.12 v. 0.46 ±0.07; P<0.01).There were striking differences in EF between those patientswith anterior and those with inferior infarction. Mean EF forthose surviving primary VF after transmural anterior infarction(0.23±0.06) was lower than those who had primary VF aftertransmural inferior infarction (0.43±0.06; P<0.01J.Normal left ventricular function was seen in four individualswho developed no further complications. Recurrent primary ventriculararrhythmia was seen v only in those individuals subsequentlyshown to have reduced EF. Low EF (< 0-35) was seen in 12patients with primary VF in the context of anterior infarction,five developed breakthrough ventricular arrhythmias despitetherapy and in a limited follow-up period, three have died.     

Effects of captopril on ventricular arrhythmias in the early and late phase of suspected acute myocardial infarction: Randomized, placebo-controlled substudy of ISIS-4

The antiarrhythmic effect of oral captopril was studied duringthe early (day 3) and late (day 14) phase of acute myocardialinfarction among 304 patients in a randomized placebo-controlledsubstudy of ISIS-4. Ventricular arrhythmias (ventricular ectopic beats per hour)occurred significantly less frequently among captopril-allocatedpatients than among those allocated placebo at day 3 (logarithmicscale: 0·48 ± 0·8 captopril vs 0·84± 1·3 placebo; P<0·003) and at day 14(0·51 ± 1·0 vs 0·77 ± 1·3;P<0·05). The number of patients with frequent ventriculararrhythmias (more than 10 ventricular ectopic beats per hour)was also significantly lower among those allocated captoprilat day 3 (7·3% vs 14·4% P<0·05) andat day 14 (7·3% vs 14·8%; P<0·05). These results support the hypothesis that the activation ofthe renin-angiotensin-aldosterone and sympathetic system mayunderlie heart rhythm disturbances in acute myocardial infarction,and that early use of converting enzyme inhibitor therapy mayameliorate these disturbances. (Eur Heart J 1996; 17: 1506–1510)     

Prognostic value of exercise radionucide angiography in low risk acute myocardial infarction survivors

Patients with an uneventful course during hospital stay, whichrepresent from 30 to 50% of all myocardial infarction survivors,still have an incidence of new coronary events up to 7% duringthe first year of follow-up. To assess the value of radionuclideangiography in predicting new coronary events in this low riskpopulation, 93 patients without evidence of left ventricularfailure or recurrent postinfarction angina underwent rest andexercise radionuclide angiography and treadmill exercise testingbefore hospital discharge. During follow-up (16 ± 5 months, range 12 to 32) 14 patientsdeveloped new coronary events: two patients died, four had anew myocardial infarction and the remaining eight had unstableangina. There were no differences regarding clinical variables,the results of the exercise test and the resting ejection fraction,between patients with or without new coronary events; however,patients without events during follow-up exercised longer duringboth exercise treadmill test and exercise radionuclide angiography.Resting end-diastolic and end-systolic volume indexes were higherin patients presenting coronary events (122 ± 50 vs 92± 32 ml. m^–1 P <0.05, 69 ± 47 vs 47 ±26 ml. m^–2, P <0.05). These patients also had a higherincidence of wall motion abnormalities in more than one area(64 vs 28%, P <0.02). During exercise, ejection fractionincreased significantly in patients with an uneventful outcome(49 ± 13 to 56 ± 14%, P <0.01), while it didnot change in their counterparts (46 ± 14 to 45 ±14%, NS). Thus, the proportion of patients in whom the ejectionfraction decreased > 5% during exercise was higher amongpatients developing new coronary events during follow-up (43vs 10%, P < 0.01). There were no differences regarding exerciseventricular volumes. Multivariate analysis, using data from the clinical course andresting radionuclide angiography, identified presence of extensive(> one area) regional wall motion abnormalities (P <0.01)and end-diastolic volume index (P <0.03) as independent predictorsof prognosis. When data from exercise testing and exercise radionuclideangiography were added, a decrease in exercise ejection fraction> 5% (P < 0.005) and end-systolic volume index at rest(P <005) were identified as predictors of new coronary events.Comparison of sensitivity and specificity of each regressionequation, using ROC curves, also indicated that exercise radionuclideangiography added information to rest variables. In conclusion, rest and exercise radionuclide angiography arehelpful in evaluating the prognosis in patients with an uneventfulcourse after myocardial infarction. In this low risk group,exercise radionuclide angiography showed better prognostic valuethan the exercise test.     

Functional role of microvascular integrity in patients with infarct-related artery patency after acute myocardial infarction

AIMS: The study was set up to evaluate the functional role of post-infarctpreserved microvascular integrity. Low dose dobutamine echocardiographyand myocardial contrast echocardiography were used to studypatients before hospital discharge who had suffered a recentmyocardial infarction and had a patent infarct-related artery(TIMI flow grade 3). METHOD: In the dysfunctioning infarct area, the wall motion score indexwas calculated at baseline, during the dobutamine infusion andat the 3 month follow-up echocardiogram; contrast echocardiographywas performed at the time of coronary angiography, before hospitaldischarge. RESULTS: In patients with more than 50% of the dysfunctioning infarctarea opacified at contrast echocardiography (group A), regionalwall motion score index decreased, compared to baseline, duringthe dobutamine infusion (1·97 ± 0·78 vs2·5 ± 0·35 at baseline; P<0·001)and at follow-up echocardiography (1·83 ± 0·63vs 2·5 ± 0·35 at baseline; P<0·001).In patients with less extensive microvascular integrity as revealedby contrast echocardiography (group B), regional wall motionscore index did not decrease from baseline during either thedobutamine infusion (2·73 ± 0·21 vs 2·81± 0·20 at baseline; P=ns) or at follow-up (2·81± 0·20 vs 2·81 ± 0·20 atbaseline; P=ns). CONCLUSION: In patients with post-infarct dysfunctioning myocardium buta patent infarct-related artery, microvascular integrity, asassessed by myocardial contrast echocardiography, is an indicatorof myocardial viability in terms of preserved contractile reserve,as demonstrated by dobutamine infusion and functional recoveryat follow-up.     

Prognostic value of thallium-201 myocardial scintigraphy after atrial transoesophageal pacing in patients with suspected coronary artery disease

Fifty-five patients with suspected coronary artery disease underwentplanar thallium-201 myocardial scintigraphy after atrial transoesophagealpacing. Coronary angiography was carried out in all patients.Eighteen patients had no myocardial infarction, but a greaterthan 50% narrowing of at least one main vessel: initial hypoperfusionwith redistribution at 4 h occurred in 16 patients (sensitivity89%). Twenty-one patients had had a previous myocardial infarction:a reversible thallium defect was observed in 12 patients andan irreversible defect in the nine remaining patients. Sixteenpatients had normal coronary arteries: a reversible thalliumdefect was observed in three patients (specflcity 81%). Aftera mean follow-up of 22±13 months (range 6 to 40), 23cardiac events occurred: cardiac death in one patient, unstableangina in three, and revascularization procedures for recurrentangina despite medical therapy in 19 (coronary artery bypasssurgery in 7 and coronary angioplasty in 12). By univariateanalysis, the predictors of future cardiac events were a historyof previous myocardial infarction (odds ratio 55, P<0.02)multivessel coronary artery disease (odds ratio 9.6, P<0.0002),angina during atrial pacing (odds ratio 5.1, P<0.05), abnormalscintigraphy (odds ratio 17.1, P<0.001) and reversible perfusiondefect after pacing (odds ratio 7.9, P<0.002). By multivariateanalysis, multivessel disease (P<0.004) and reversible perfusiondefect after pacing (P<0.02) were the only independent predictorsof future cardiac events. In conclusion, thallium-201 myocardial scintigraphy after transoesophagealatrial pacing is accurate for the diagnosis and prognosis ofpatients with suspected coronary artery disease, and may beundertaken in patients unable to perform exercise stress testing.     

Functional characteristics of myocardial bridging: A combined angiographic and intracoronary Doppler flow study

AIMS: Combined quantitative coronary angiography and intracoronaryDoppler flow velocity measurements were performed to study theunderlying haemodynamic mechanisms leading to myocardial ischaemiain patients with myocardial bridging in the absence of coronaryartery disease. METHODS AND RESULTS: In 42 symptomatic patients with myocardial bridging of the leftanterior descending coronary artery, quantitative coronary angiographywas used to measure absolute and relative vessel diameters duringsystole and diastole. In 14 patients, serial frame-by-framediameter quantification during a complete cardiac cycle wasperformed. Intracoronary blood flow velocities were determinedusing a 0·014 inch Doppler flow guide wire proximal,within, and distal to myocardial bridges, and coronary flowreserve was calculated. Quantitative coronary angiography revealeda maximal systolic lumen diameter reduction of 71 ± 16%with a persistent diameter reduction of 35 ± 13% duringmid-diastole. Flow velocities revealed increased average diastolicpeak flow velocities within myocardial bridges of 38·6± 19 cm. s^–1 vs 22·4 ± 7·7cm. s^–1 proximal and 18·6±4·6cm.s^–1 distal (P<0·001), which increased duringrapid pacing (64·7 ± 25 cm. s^–1, P<0·001vs baseline). Coronary flow reserve distal to myocardial bridgeswas 2·3 ± 0·9 (vs 2·9 ± 0·9proximal, P<0·05). There was a characteristic Dopplerflow profile within myocardial bridges with an early diastolicovershoot, which was further augmented during rapid pacing. CONCLUSION: Myocardial bridging is characterized by a delay in diastoliclumen gain and a concomitant increase in diastolic intracoronaryDoppler flow velocities, which are enhanced by rapid pacing.In combination with a reduced coronary flow reserve and anginalsymptoms these findings support the concept of a haemodynamicallysignificant obstruction to coronary flow due to myocardial bridgingin a selected subset of patients.     

Dipyridamole echocardiography evaluation of acute inferior myocardial infarction with concomitant anterior ST segment depression

The significance of anterior ST segment depression in inferioracute myocardial infarction (AMI) remains controversial. Theaim of this study was to relate precordial ST segment depressionto the topography of residual myocardial ischaemia, with myocardialmapping of the asynergic area and coronary anatomy. Twenty-fivepatients with first inferior AMI (15 patients with anteriorST segment depression: group A and 10 patients without anteriorST segment shift: group B), all underwent: (1) electrocardiographicevaluation on admission to the Coronary Care Unit and at 24h intervals thereafter; (2) 2D-echocardiographic study within3 h of CCU admission: (3) dipyridamole echocardiographic test(DET) (doses of dipyridamole up to 0.84 mg.kg^–1 i.v. over10 min) 4 days after AMI; (4) coronary arteriography within14 days from AMI. To assess regional left ventricular wall motion,a 16 segment model was used and a wall motion score index (WMSI)was derived. The results of DET were correlated to the anatomyof the infarct-related vessel. Compared to group B, group Apatients showed a significantly greater maximal ST segment elevationin inferior limb leads (lead III: 3.9±1.9 mm vs 2.2±1.1mm, P<0.05; aVF: 3.5±13 mm vs 1.7±0.8 mm, P<0.001).Group A patients showed greater WMSI (1.35±0.22 vs 117±0.12,P<0.05), with more frequent postero-lateral wall involvement(72% vs 20%, P<0.05). No patient of either group showed asynergyof the anterior, anterolateral or anteroseptal segments. Nodifferences in the distribution of coronary artery disease wereobserved. Left anterior descending coronary artery disease waspresent in only three patients (20%) in group A and in one patientin group B. DET was positive in eight patients (53%) in groupA and in three (30%) in group B (P = statistically not significant).In all patients DET induced new wall motion abnormalities locatedin the territory of the infarct-related artery. None of thepatients developed new wall motion abnormalities remote fromthe infarct zone or adjacent to the infarct zone, but locatedin different vascular regions. In conclusion, anterior ST segmentdepression in inferior A MI appears to indicate a more extensivearea of asynergy, with frequent involvement of the posterolateralwall. The topography of DET-induced residual myocardial ischaemiadoes not support the hypothesis of concomitant anterior ischaemia.     

Beneficial effect of enalapril on left ventricular remodelling in patients with a severe residual stenosis after acute anterior wall infarction

OBJECTIVE: The present study was designed to evaluate the effects of earlyangiotensin converting enzyme (ACE) inhibition on left ventricularenlargement in patients with anterior wall infarction followingreperfusion therapy. METHODS: Seventy-one consecutive patients with an anterior wall myocardialinfarction were randomly allocated to enalapril (n=36) or placebo(n=35). All patients received either thrombolytic therapy (n=46)or underwent primary coronary angioplasty (n=25). Medicationwas started within 48 h admission to hospital and continuedfor 48 weeks. The process of left ventricular remodelling wasassessed with two-dimensional echocardiography at 3 weeks and1 year after the acute onset, and was related to the severityof the residual stenosis of the infarct-related artery. RESULTS: Baseline left ventricular ejection fraction was 39·2±8·7%.During the study period, left ventricular end-diastolic volumeindex increased from 48·2±9·9 ml. m^–2to 54·6±12·2 ml. m^–2 at 3 weeks,and to 59·4±170 ml. m^–2 after 1 year incontrol patients (P<0·001). In the enalapril-treatedpatients, left ventricular end-diastolic volume index increasedfrom 50·0±16·1 to 57·7±19·3ml. m^–2 at 3 weeks, and to 61·9±22·7ml. m^–2 after 1 year (P<0·001). Both at 3 weeksand after 1 year, no overall differences in left ventricularvolumes were observed between the enalapril and the placebogroup (both ns). However, patients with a residual stenosisseverity of 70% in the infarct-related artery (n=43) showedsignificant attenuation of remodelling by enalapril (n=22) whencompared to placebo (n=21). In patients on enalapril, left ventricularend-diastolic volume index increased from 470±130 to53·7±17·7 ml. m^–2 compared to 48·0±9·6to 60·3±16·3 ml . m^–2 in controlpatients (P<0·03). Also diastolic filling parameterswere significantly improved in patients with 70% residual stenosis. CONCLUSION: In patients with an anterior wall infarction and a severe residualinfarct-related coronary artery stenosis following reperfusion,treatment with enalapril prevents the process of left ventricularremodelling. As left ventricular dilatation is an early processwe suggest that treatment with ACE inhibition should be startedas soon as possible in this group of patients.     

Determinants of exercise capacity in patients with coronary artery disease and mild to moderate systolic dysfunction: Role of heart rate and diastolic filling abnormalities

BACKGROUND: To test the hypothesis that diastolic filling abnormalitiesare an important cause of exercise limitation in some patientswith coronary artery disease we assessed the factors limitingexercise capacity in a group of patients with coronary arterydisease in whom exercise limitation was greater than expectedfrom the degree of resting left ventricular systolic dysfunction. METHODS AND RESULTS: We assessed the relationship between exercise capacity (maximaloxygen consumption) during erect cycle ergometry, heart rate,radionuclide indi ces of left ventricular systolic function(ejection fraction) and diastolic filling (peak filling rate,and time to peak filling) during semi-erect cycle ergometryin 20 patients (15 male, five female) who were aged 42–72years (mean 61 years) and had angiographically proven coronaryartery disease and evidence of reversible myocardial ischaemiaon thallium scintigraphy. All patients exhibited marked exerciselimitation (maximal oxygen consumption 8.7–22.4 ml. min^–1.kg^–1— mean 15.9 ml. kg^–1. min^–1, whichwas 611 ± 16% of age and gender predicted maxi mum) dueto breathlessness or fatigue rather than angina, in spite ofa mean ejection fraction for the group of 465% (range 30–67%).We also compared the diastolic filling characteristics of thesepatients during exercise with 10 healthy controls (age 38–66,mean 58 years; eight male, two female). Comparing diastolicfilling characteristics, peak filling rate was higher and timeto peak filling shorter both at rest and peak exercise in controlsthan patients (peak filling rate 3.1± 0.5 vs 2.2±0.9 EDV. s^–1 P =0.01 at rest and 8.3± 0.8 vs 5.2±1.9 EDV. s^–1 , P< 0.0000l on exercise; time to peakfilling 115.2± 29.8 vs 228.9± 71.7 ms, p< 0.0001.atrest and 52.8± 16.2 vs 139.6± 4.48 ms, P<0.0000lon exercise respectively). On univariate analysis in the patientsstudied, maximal oxygen consumption was correlated with peakheart rate (r=0.45 P=0.04), peak exercise time to peak filling(r=– 0.85 P< 0.0001 peak exercise peak filling rate(r = 0.58, P=0.019), and the relative increase in cardiac outputi.e. cardiac output peak/cardiac output rest (r=0.58, P=0.008).There was no correlation between maximal oxygen consumptionand resting indices of diastolic filling (peak filling rateand time to peak filling) or with resting or peak exercise ejectionfraction. On multiple regression analysis, only peak exercisetime to peak filling was significantly related to maximal oxygenconsumption. CONCLUSION: We have observed a strong correlation between exercise capacityand indices of exercise left ventricular diastolic filling,and have confirmed previous studies showing a poor correlationwith resting and exercise indices of systolic function and restingdiastolic filling, in patients with coronary artery disease.     

Changes in platelet size and count in unstable angina compared to stable angina or non-cardiac chest pain

Aims An increase in platelet aggregability is associated withunstable angina and myocardial infarction. Platelet size andactivity correlate and mean platelet volume was found to beincreased before acute myocardial infarction. We measured themean platelet volume and platelet count in patients with stableangina, unstable angina and non-cardiac chest pain. Methods and results We studied 981 patients (734 men; 247 women)defined clinically as stable angina (n=688), unstable angina(n=108) and unstable angina requiring immediate angioplasty(n=52). After coronary angiography the patients were subdividedinto single (n=269), double (n=304) and triple-vessel disease(n=311) and the control group of non-cardiac chest pain (n=97).There was no significant difference in platelet count betweenthe control group and patients with 1, 2, or 3-vessel disease.However, the platelet size in patients with coronary arterydisease was significantly larger (single: 8·7±1·19fl;double: 8·7±1·12fl; triple-vessel disease:8·8±1·18fl) than the control group (8·2±0·95fl)(P<0·01). Patients with stable angina similarly hadno significant difference in platelet count compared to thecontrol group but did have a significantly increased mean plateletvolume (8·7±1·13;P<0·01). Incontrast, patients with unstable angina had a decreased plateletcount (245±56x10/l) compared to either stable angina(262±62x10/l;P<0·05) or the control group (261±58x10/l;P<0·05);furthermore, the mean platelet volume (9·4±1·23fl)was significantly greater than for stable angina (P<0·01).Patients with unstable angina requiring immediate PTCA had aneven lower platelet count (231±55x10/l) and higher meanplatelet volume (10·4±1·03fl) (P<0·01)than the rest of the population with unstable angina. Conclusions In stable angina the platelet count is unchangedcompared to patients with normal coronary arteries but the plateletsize is increased. However, in unstable angina there is a decreasein platelet count and an even larger increase in platelet size.We interpret this as meaning that unstable angina might be associatedor preceded by an increase in platelet destruction rate thatis not completely compensated for by an increase in plateletproduction rate. The large, more reactive platelets might becausally related to an ongoing coronary artery obstruction inunstable angina.     

Heart rate variability as a means of assessing prognosis after acute myocardial infarction: A 3-year follow-up study

AIMS: The present study evaluated the prognostic value of heart ratevariability after acute myocardial infarction in comparisonwith other known risk factors. The cut-off points that maximizedthe hazards ratio were also explored. PATIENTS AND METHODS: Heart rate variability was assessed with 24 h ambulatory electrocardiographyin 74 patients with acute myocardial infarction, 4±2days after hospital admission and in 24 healthy controls. Patientswere followed for 36±15 months. RESULTS: During follow-up, 18 patients died, nine suffered a non-fatalinfarction and 20 underwent revascularization procedures. Heartrate variability was higher in survivors than in non-survivors(P=0·0005) This difference was found at higher statisticallevels when comparing non-survivors vs controls (P=0·0002)A similar statistically significant difference was also foundbetween survivors vs controls (P=0·04). Patients sufferingnon-fatal infarction and cardiac events (defined as death, non-fatalinfarction or revascularization) had a lower heart rate variabilitythan those without (P=0·03 and P=0·03, respectively).With multivariate regression analysis, decreased heart ratevari ability independently predicted mortality and death ornon-fatal infarction. The presence of a left ventricular ejectionfraction <40% and a history of systemic hypertension were,however, stronger predictors. The cut-off points that maximizedthe hazards ratio using the Cox model differed from those reportedby others. CONCLUSIONS: Decreased heart rate variability independently predicted poorprognosis after myocardial infarction. However, the cut-offpoints that should be used in clinical practice are still amatter for further investigation.     

Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangement of coronary microvascular function

Non-sustained ventricular tachycardia on Holter and syncopehave been considered risk factors for sudden death in hypertrophiccardiomyopathy. AIMS: In these patients the coronary vasodilator reserve is impaireddespite normal coronaries, so we evaluated the correlation betweenthe severity of coronary vasodilator reserve impairment andthe occurrence of syncope and non-sustained ventricular tachycardia. METHODS AND RESULTS: Eighty-four patients with hypertrophic cardiomyopathy (62 males,age 43±12 years) had a two-dimensional echocardiographicstudy and a 48-h Holter. Myocardial blood flow was measuredby positron emission tomography, at baseline and after dipyridamole,and the coronary vasodilator reserve was computed as dipyridamolemyocardial blood flow/baseline myocardial blood flow. In 27patients, subendocardial and subepicardial myocardial bloodflow was measured in the septum and the subendocardial/subepicardialratio was computed. Twenty of 84 patients had at least one syncopalepisode, and 26 had at least one run of non-sustained ventriculartachycardia on Holter. Baseline and dipyridamole myocardialblood flow, coronary vasodilator reserve, and baseline and dipyridamolesubendocardial/subepicardial myocardial blood flow ratio weresimilar in patients with and without syncope and with and withoutnon-sustained ventricular tachycardia on Holter. However, patientswith non-sustained ventricular tachycardia had larger left ventricularend-diastolic (47±6 vs 44±5 mm, P<0·05)and end-systolic diameters (30±6 vs 27±4 mm, P<0·05). CONCLUSIONS: (1) Coronary vasodilation is not more severely impaired in patientswith hypertrophic cardiomyopathy and syncope or non-sustainedventricular tachycardia. (2) The left ventricle is more dilatedin hypertrophic cardiomyopathy with non-sustained ventriculartachycardia.     

Degree of residual stenosis of the infarct-related artery. Another variable affecting recovery of regional function after thrombolysis

Aims The aim of this study was to analyse the relationship betweeninfarct-related artery residual stenosis, assessed by quantitativecoronary angiography, and left ventricular function changesduring the in-hospital period in patients with acute myocardialinfarction undergoing thrombolytic treatment. Methods and Results The study population consisted of 90 patients with acute myocardialinfarction treated with thrombolysis within 6h of the onsetof symptoms. Left ventricular function was serially assessedby an echocardiographic asynergy score (before thrombolysisand pre-discharge). Left ventricular end-diastolic and end-systolicvolumes were also calculated. Coronary stenosis was evaluatedby computer-assisted videodensitometric analysis at pre-dischargecoronary angiography. Three subgroups were identified on thebasis of left ventricular function changes: 25 patients (GroupA) with regional myocardial improvement (echo score from 7·5±3·5to 4·3±3·2), 51 (Group B) with no variationin echo score (4·8±2·7) and 14 (Group C)with myo-cardial regional worsening (echo score from 4·4±2·1to 8·8±2·4). Group A patients exhibiteda very high incidence of infarct-related artery patency (23/25patients, 92%) vs 71% with unchanged (Group B) and 14% (GroupC) with worsening regional left ventricular function (P<0·001).Subdivision of the study population on the basis of residualstenosis severity showed that a significant improvement in leftventricular function was present only in the subgroup with residualstenosis <75% (echo score from 5·2±3·4to 3·6±2·9,P<0·001). Conclusion These results support the important role exerted by completecoronary patency after thrombolysis in inducing left ventricularfunction recovery, and the poor functional improvement in patientswith incomplete coronary patency.     

Severe mitral regurgitation complicating acute myocardial infarction: Clinical and angiographic differences between patients with and without papillary muscle rupture

AIMS: To assess the differential clinical and angiographic characteristicsof patients with severe mitral regurgitation related (n=31)or unrelated (n=16) to papillary muscle rupture complicatingacute myocardial infarction. MEHTODS AND RESULTS: The clinical and angiographic features of patients with myocardialinfarction and severe mitral regurgitation were evaluated. Patientswith papillary muscle rupture were older (67 vs 60 years, P>0·005)and had a lower rate of diabetes (7% vs 38%, P>0·005)and of previous angina or infarction (24% vs 50%, P>0·05).Frequency of inferior infarction was high and comparable inboth groups (papillary muscle rupture, 72% vs non-papillarymuscle rupture, 88%, ns) whereas in-hospital rate of angina/infarctextension prior to mitral regurgitation, also high, tended tobe higher in patients without than in those with papillary musclerupture (67% vs 39%, ns). Incidence of multivessel disease tendedto be higher in patients without papillary muscle rupture (87%vs 56%, P>0·06) and they had a lower ejection fraction(46 ± 15 vs 61 ± 14%, P>0·03), whereasthe culprit artery was mainly the right or the circumflex coronaryartery in both groups (papillary muscle rupture, 100% vs nonpapillary muscle rupture, 93%, ns). Valve replacement was performedearlier in patients with papillary muscle rupture (1(1; 14)vs 25 (5; 45) days, median, P>0·002) but was associatedwith a similar mortality (papillary muscle rupture 11/24, 46%vs non-papillary muscle rupture, 7/15, 47%, ns). The main causeof death was cardiogenic shock in patients without papillarymuscle rupture (5/7, 71%), and respiratory insufficiency-sepsisin those with papillary muscle rupture (7/11, 64%). CONCLUSIONS: Severe mitral regurgitation in myocardial infarction with orwithout papillary muscle rupture is mostly related to inferiorinfarction and often follows reinfarction, particularly in non-papillarymuscle rupture cases. The main contributors to surgical mortalityappear to be respiratory insufficiency in patients with papillarymuscle rupture and cardiogenic shock, facilitated by a lowerejection fraction, a higher frequency of diabetes and more extensivecoronary disease, in patients without papillary muscle rupture.     

Significance of Q-wave regression after anterior wall acute myocardial infarction

Aims This study was conducted to clarify the significance of abnormalQ-wave regression in anterior wall acute myocardial infarction. Methods A total of 74 patients who presented with a first anterior wallacute myocardial infarction within 6h of onset were dividedinto two groups according to the presence (group A, n=29) orabsence (group B, n=45) of regression of abnormal Q waves. Regressionof abnormal Q waves was defined as the disappearance of theQ wave and the reappearance of the r wave 0·1mV in atleast one of leads I, aVL, and V₁to V₆. Results Emergency coronary arteriography revealed that group A had ahigher incidence of spontaneous recanalization or good collateralcirculation than group B (55% vs 31%,P<0·05). Peakcreatine kinase activity tended to be lower in group A thanin group B (2358±1796 vs 3092±1946IU.L^–1,P=0·09).Group A had a greater left ventricular ejection fraction andbetter regional wall motion at 1 and 6 months after acute myocardialinfarction than group B. The degree of improvement of left ventricularejection fraction and regional wall motion between 1 and 6 monthsafter acute myocardial infarction was significantly greaterin group A than in group B. Conclusion Patients with anterior wall acute myocardial infarction showingQ-wave regression had a trend towards a smaller amount of necroticmyocardium and a significantly larger amount of stunned myocardium.     

Significance of ST-segment elevation during dobutamine-stress echocardiography in patients with acute myocardial infarction treated with thrombolysis

BACKGROUND: Stress-induced ST-segment elevation in patients with recentmyocardial infarction treated with thrombolysis has not beenextensively investigated. According to the results of previousstudies it may represent residual myocardial ischaemia or dyskinesiain the infarcted region. The aim of the study was to analysethe significance of dobutamine-induced ST-segment elevationin the infarcted area in a consecutive group of patients (n=42,41 men, mean age 53 ± 7 years) with a first acute myocardialinfarction treated with thrombolysis within 6 h from symptomsonset. METHODS AND RESULTS: All patients underwent dobutaminestress echocardiography (upto 40 µg. kg^–1. min^–1+ atropine) 7 ±3 days from the acute event and coronary arteriography within1 month from the test. Significant ST-segment elevation wasdefined as a shift 1 mm during dobutamine compared to baselinein at least two contiguous infarct-related leads; a correlationwas made between the site of ST-segment elevation and wall motionchanges during dobutamine. Dobutamine-induced ST-segment elevationin 23/42(55%) patients (group 1) while no changes were observedin 19/23 (45%) patients (group 2). Compared to group 2, group1 patients showed a higher asynergy score index (1·72± 0·24 vs 1·50 ± 0·32, P<0·02)and a higher number of asynergic segments (5·04 ±1·9 vs 4·11 ± 1·8), at baseline,a higher incidence of baseline and/or stressinduced dyskinesia(39 vs 10%, P<0·05) in the infarct-related regionand a higher percentage of occluded infarct-related arteries(48 vs 0%, P<0·001). In the 42 patients studied, asignificant correlation was found between baseline ST-segmentelevation and baseline asynergy score index (RS=0·56,P<000l) and between ST-segment elevation and asynergy scoreindex at peak stress (RS=0·55, P<0·001). Theincidence of reversible wall motion abnormalities indicativeof myocardial viability and residual myocardial ischaemia wassimilar in the two groups (87 vs 84% and 74 vs 68%, respectively),while the number of segments with irreversible akinesia indicativeof myocardial necrosis was higher in group 1 compared to group2 (1·5 ± 14 vs 0·9 ± 1·4).Among the 23 patients of group 1 with dobutamine-induced ST-segmentelevation, six had no reversible wall motion abnormalities indicativeof myocardial ischaemia; of the 17 patients with myocardialischaemia, 11 had 50% and six had 50% of basally asynergic segmentsshowing reversible wall motion abnormalities. CONCLUSIONS: In patients with recent thrombolyzed myocardial infarction dobutamine-inducedST-segment elevation is associated with a larger akinetic areain basal conditions and either with reversible wall motion abnormalitiesindicative of myocardial ischaemia or with irreversible or minimallyreversible wall motion abnormalities in the infarct area duringthe test. Thus, dobutamine echocardiography provides usefulinformation for the interpretation of stress-induced ST-segmentelevation and clinical management of these patients.     

Coronary anatomy and left ventricular ejection fraction in patients with type 2 diabetes admitted for elective coronary angiography

Patients with diabetes mellitus (DM) have more severe coronary artery disease and a two‐ to fourfold higher risk for myocardial infarction and death as compared to patients without DM. In this study, we analyzed coronary anatomy, left ventricular ejection fraction, and cardiac risk factors in patients with DM referred for coronary angiography and compared them with findings in nondiabetic patients. Coronary anatomy was assessed in a total of 6,234 patients and left ventricular ejection fraction in a subset of 4,767 (76.5%) patients. Diabetic patients (n = 641) were older (60.8 ± 9.6 vs. 58.5 ± 10.5 years; P < 0.0001) and had higher rates of hypertension (65% vs. 47%; P < 0.0001). Three‐vessel disease (DM 44.7% vs. no DM 25.4%; P < 0.0001) and reduced left ventricular ejection fraction (DM 58.4% ± 15.2 vs. no DM 63.9% ± 13.2; P < 0.0001) were significantly associated with DM. After adjustment for age and other vascular risk factors, the presence of DM was associated with a higher atherosclerotic burden. We conclude that advanced coronary heart disease and left ventricular dysfunction are highly prevalent in diabetic patients, independent of age and other cardiovascular risk factors. Thus, cardiac assessment in diabetic patients should, in addition to optimal diabetic control, involve screening for left ventricular dysfunction. Cathet Cardiovasc Intervent 2004;62:432–468. © 2004 Wiley‐Liss, Inc.