The effect of verapamil on myocardial exchange of free fatty acids, citrate, lactate and glucose in coronary artery disease

Twelve patients with coronary artery stenosis (> 50% diameterreduction) underwent two identical periods of atrial pacingbefore and after i. v. verapamil (0.1 mg/kg). Myocardial exchangesof free fatty acids (FFA), citrate, lactate and glucose wereevaluated from measurements of arterio-coronary sinus differences(n = 12) and coronary sinus blood flow (CSBF) (n = 9). Beforeverapamil 11 patients developed angina. Verapamil abolishedpain in seven and improved pacing time to angina in four patients.After verapamil, aortic pressure decreased (P < 0.05), whilethe rate pressure product remained unchanged during rest andpacing. Verapamil decreased CSBF by 20% (P<0.05) during pacing,and increased oxygen extraction both during pacing and recovery.During pacing verapamil increased net FFA extraction (P<0.01)and uptake (1 to 8 µmol/min P<0.05), and decreasedglucose extraction (P<0.05) and uptake (22 to 11 µmol/min P< 0.02. Verapamil increased myocardial citrate releaseduring pacing (P < 0.05), suggesting a citrate inhibitionof glycolysis as a possible mechanism of the inhibited glucoseuptake. During pacing, verapamil reduced lactate release inseven patients (P<0.05) and decreased lactate extractionin five patients (P<0.05). The results suggest that verapamilmediates its beneficial effect on pacing-induced angina, inpart by changing substrate utilization of the ischaemic myocardiumin man towards that of normal heart.     

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.     

A comparison of nisoldipine and nifedipine, in combination with atenolol, in the management of myocardial ischaemia

The effects of the addition of slow-release nifedipine 20 mgtwice daily and nisoldipine 10 mg twice daily to atenolol monotherapywere compared in a double-blind placebo-controlled study of24 patients with chronic stable angina pectoris. Neither nisoldipinenor nifedipine was associated with significant subjective benefitat these doses. Two hours post-dosing, exercise capacity improvedafter both nisoldipine (duration+37 s, P<0.01; time to angina+67s, P<0.01; time to sign ST depression+60 s, P<0.01) andnifedipine (duration +21 s, ns; time to angina+56 s, P<0.05;time to significant ST depression+49 s P<0.05) However, thisimprovement was not maintained 12 h post-dosing. Ambulatorymonitoring did not demonstrate a sign reduction in the amountof silent or total ischaemia following the addition of eithernifedipine or nisoldipine to atenolol monotherapy. There wasno significant difference between nifedipine and nisoldipinein any parameter tested. In conclusion, like slow-release n 20 mg, the effective durationof anti-ischaemic action of nisoldipine 10 mg is less than 12h. Since several patients experienced vasodilatory unwantedeffects, more frequent administration rather than larger individualdoses may be desirable to achieve a clinical response.     

Ischaemic threshold and haemodynamic changes during angina at rest in patients with unstable angina

To examine whether increases in heart rate might be a commontrigger of angina at rest, changes in heart rate, blood pressureand rate-pressure product during pain were compared with theischaemic threshold (heart rate with ST segment shift >=1 mm), determined by atrial pacing, in 272 patients with unstableangina. During an average of 5.9±5.2 episodes of angina,heart rate was comparable to control values (77.0±14.5vs 75.2±11.5, beats. min^–1, ns) and significantlylower than the ischaemic threshold (147.9±22.9, P <0.00001).The rate-pressure product was also lower (955±183 vs2033±369, x 10, P <0.00001). Heart rate during restangina was lower than the ischaemic threshold even when we consideredonly patients with ST depression during pain (n: 71, 81.4±16.0 vs 132.8±21.4, P<0.00001), those with three-vesseldisease (n: 43, 79.9±15.9 vs 136.9±22.0, P <0.00001), or those with a low ischaemic threshold (= <130beats. min, n: 78, 77.0±14.9 vs 118.3±10.7, P<0.00001).In 154 patients in whom a second pacing test was performed theresponse was reproducible in 137 cases (89%). Thus, heart rate barely changes during angina at rest in patientswith unstable angina and is consistently much lower than theischaemic threshold. These findings support the concept thatincreases in heart rate are an unlikely trigger of ischaemiaat rest, even in patients with markedly reduced coronary reserve.     

Beneficial effect of enhanced myocardial carbohydrate utilisation after oxfenicine (L-hydroxyphenylglycine) in angina pectoris

Although the major myocardial energy supply comes from oxidationof lipid, carbohydrate requires less oxygen for the same energyyield. Oxfenicine has been shown experimentally to favour carbohydrateutilisation and its effect in a dose of 3–12 mg/kg wasstudied in 18 patients with obstructive coronary artery disease,both at rest and during angina induced by rapid atrial pacing.No major haemodynamic changes or side effects were observedafter the drug. The mean pacing time to angina was significantlyincreased from 289 ± 33 s to 360 ± 35 s (P <0.05) and during pacing, myocardial oxygen consumption fell.After the drug there was a significant increase in myocardialextraction of carbohydrate in the form of lactate, pyruvateand glucose during pacing and in contrast, the myocardial extractionof free fatty acids fell significantly. This increase in myocardialcarbohydrate extraction associated with a reduced myocardialoxygen consumption, is of potential value not only in the treatmentof angina pectoris, but also in the early phases of acute myocardialinfarction.     

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.     

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     

Assessment of the influence of spinal cord stimulation on left ventricular function in patients with severe angina pectoris: an echocardiographic study

Patients with severe, widespread coronary atherosclerosis andpatients who have undergone several coronary artery bypass operationsare often poor candidates for coronary bypass surgery (CABG).Spinal cord stimulation (SCS) has been shown to have an anti-anginaleffect that is probably associated with an anti-ischaemic effect.In the present investigation, 15 patients with severe angina(mean age 64 years, range 49–71) were studied. All patientshad a history of intractable angina pectoris despite optimalmedical treatment and previous coronary bypass operation. Thepatients had multi-vessel disease and graft occlusion or graftstenosis on postoperative coronary angiograms. Left ventricular function was assessed echocardiographicallyat rest and during provocation with adenosine infusion in acontrol session without treatment and during treatment withSCS. The recovery time was at least 3h. The decrease in the ejection fraction during adenosine infusionwas more pronounced in the control situation (44 to 37%; P<0.05)than during SCS (48 to 44%; ns), and the time to echocardiographicsigns of dysfunction and to angina/pain during adenosine infusionwas significantly prolonged during SCS (P<0.001). In addition,the recovery time for these parameters was shorter during SCS(Plt;0.001). It is concluded that the deterioration in left ventricular functionduring adenosine provocation was less pronounced with SCS thanwithout. This possible anti-ischaemic effect is in agreementwith results from earlier studies.     

Long-term outcome of patients with incomplete vs complete revascularization after multivessel PTCA: A report from the NHLBI PTCA Registry

Background Incomplete revascularization is frequently the goalas well as the final outcome in patients with multivessel coronarydisease undergoing PTCA. However, the long-term impact of incompleterevascularization is not known and this common PTCA strategydeserves further scrutiny. Methods and results Complete revascularization was achievedin 132 of 757 patients with multivessel disease in the 1985–86NHLBI PTCA Registry. Compared to patients in whom complete revascularizationwas achieved, patients with incomplete revascularization wereolder (P<0·05), more likely to be females (P<0·05)and to have recent myocardial infarction (P<0·05),unstable angina (P<0·001), and urgent or emergentPTCA (P<0·001). Early death, Q wave myocardial infarctionand CABG rates were higher in patients with incomplete thanin those with complete revascularization [significantly different(P<0·05) only for emergency and elective CABG]. At9 years, nearly twice as many patients with incomplete revascularizationexperienced recurrent angina (19% vs 10% for patients with completerevascularization,P<0·05). Patients with completerevascularization were more likely to undergo repeat PTCA thanthose with incomplete revascularization (40% vs 30%,P<0·05).Patients with incomplete revascularization were more likelyto undergo CABG than patients with complete revascularization(32% vs 14%,P<0·001; adjusted risk 2·56, 95%CI 1·60, 4·10). Among patients with incompleterevascularization, those in whom PTCA was intended but not attemptedhad the highest early event rates and late CABG rates. Finally,the adjusted risk of dying, having a Q wave myocardial infarction,recurrent angina or repeat PTCA was not different at 9-yearfollow-up among patients with and without complete revascularization. Conclusions Complete revascularization achieved by PTCA reduceslate occurrence of CABG, but not adjusted rates of death, Qwave myocardial infarction, recurrent angina, and repeat PTCAin patients with multivessel coronary disease. These data tendto support the PTCA strategy of incomplete revascularizationin patients with multivessel disease when complete revascularizationis not feasible or not planned before the procedure.     

Effects of new calcium channel blocker of niludipine on the coronary hemodynamics,diastolic properties,and metabolic responses to tachycardia stress in patients with coronary disease

A new calcium channel blocker, niludipine, was administered intravenously to nine patients with coronary artery disease in order to investigate its effects on left ventricular systolic and diastolic function, coronary sinus blood flow, and myocardial lactate metabolism. Coronary sinus pacing was performed in all patients and produced angina in six patients. Niludipine increased the resting heart rate from 75 ± 3 beats/min (mean ± SEM) to 82 ± 3 (NS) and decreased the left ventricular systolic pressure from 155 ± 4.7 mm Hg to 134 ± 2.8 (p < 0.05). Coronary sinus blood flow increased by 9%(NS). During pacing after niludipine, clinical improvement occurred in the six patients who had initially experienced angina. The extent of ischemic ST segment depression was decreased (?1.56 ± 0.27 mm to ?0.78 ± 0.38, p<0.02) and myocardial lactate metabolism was improved. When pacing was terminated, niludipine suppressed the elevation of left ventricular end-diastolic pressure compared to pretreatment values (16.2 ± 2.5 mm Hg vs 8.5 ± 0.9, p < 0.05) and decreased the left ventricular time constant T(26.4 ± 3.6 msec to 20.2 ± 2.4, p < 0.05). The results suggest that niludipine appears to be beneficial in reducing systolic and diastolic work of the left ventricle during pacing induced angina without a significant change in total coronary sinus blood flow. Niludipine appears to have less of a hypotensive and reflex tachycardic effect than nifedipine.     

Haemodynamic impact of the left ventricular pacing site during graded ischaemia in an open-chest pig model

Aims: In post-operative setting after cardiac surgery, the choiceof the optimal ventricular pacing site remains an issue, particularlyin patients with ischaemic cardiomyopathy. We aimed to investigatethe impact of the left ventricular (LV) pacing site in an animalmodel of incremental myocardial ischaemia. Methods and results: Three epicardial LV pacing leads were implanted in 10 pigs [LV1in the territory of the left anterior descending (LAD) artery,LV2 in the lateral border of this territory, LV3 in an anatomicallyopposed position]. A two-dimensional strain echocardiogram wasperformed at baseline and during two levels of incremental ischaemia,corresponding to 30 and 70% reduction of coronary flow in theLAD, during spontaneous sinus rhythm (SR) and during LV1, LV2,LV3, and multi-LV (LV1 + LV2 + LV3) pacing. At baseline (n =10), LV + dP/dt_max was decreased (P < 0.01) during LV1, LV2,LV3, and multi-LV pacing compared with SR. At first level ofischaemia (n = 7; 3 animals died from ventricular fibrillation),LV1 pacing (ischaemic area) induced a significant decrease inLV + dP/dt_max compared with SR, LV2, LV3, and multi-LV pacing(P < 0.05). At second level of ischaemia (n = 6), LV1 pacinginduced a significant decrease in LV + dP/dt_max associated withan increase in the extent of myocardium with echocardiographicpost-systolic shortening compared with SR, LV2, LV3, or multi-LVpacing (P < 0.05). In contrast, multi-LV pacing induced asignificant haemodynamic improvement compared with SR, LV1,LV2, and LV3 (P < 0.05). Conclusions: Pacing within an ischaemic area has detrimental impact on acuteglobal and regional LV function. More studies are needed toassess the impact of multi-LV pacing in chronic ischaemic conditions.     

Repeat percutaneous coronary angioplasty; clinical and angiographic follow-up in patients with stable or unstable angina pectoris

This study analyses the immediate outcome and the risk of recurrentrestenosis in patients who, at the time of repeat coronary angioplastyfor a first restenosis, had unstable (n = 50), 19%) or stable(n = 218, 81%) angina. Successful angioplasty was accomplishedin 250 (93%) patients, 222 (89%) of whom hadfollow-up angiography.Mean time from initial to repeat angioplasty was shorter (P= 0.0002) and angiographic evidence of thrombus was commoner(P = 0.0001) in the unstable group. Major complications (coronaryartery bypass grafting or myocardial infarction) were morefrequent(P <0.01) in the unstable group (6% vs 0.5%); no procedure-relateddeaths occurred. The angiographic rate of restenosis was significantlyhigher in the unstable group (61% vs 43%, P <0.05). Despitethis high rate of recurrent restenosis, most of the patientsin both groups were either asymptomatic or had atypical chestpain at follow-up. Repeat coronary angioplasty, in patients with unstable angina,has a high primary success rate but a higher risk of acute complicationsthan in patients with stable angina. The angiographic rate ofrestenosis was significantly higher in unstable than in stablepatients, however, the clinical status of most patients wasimproved at follow-up.     

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.     

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.     

Diagnostic accuracy of dobutamine stress echocardiography for detection of coronary heart disease in hypertensive patients

To compare the diagnostic accuracy between dobutamme echocardiographyand treadmill exercise electrocardiography in detecting coronaryartery disease in hypertensive patients, 43 patients withoutelectrocardiographic evidence of left ventricular hypertrophyand basal ST-T changes, who had also undergone coronary angiography,were further evaluated by dobutamine echocardiography. The patientsalso underwent treadmill exercise echocardiography. Left ventricularmass index was calculated by echocardiography. Twenty-nine patientshad coronary artery disease, of whom 22 had multi-vessel diseaseand 14 a normal coronary anatomy. Twenty-eight patients hadan increased left ventricular mass index. The sensitivitiesof dobutaniine echocardiography and exercise electrocardiographyfor detecting coronary artery disease were 93% and 72% (P=0·08)respectively, and the specificities were 100% and 29%(P<0·005),respectively. Logistic regression analysis showed exercise electrocardiographyto be a poor predictor of coronary artery disease (P<0·09)but dobutamine echocardiography was significantly better (P<0·00l).When patients with increased left ventricular mass index wereexcluded, prediction of coronary anatomy by exercise electrocardiographyimproved only marginally (P=0·4) while dobutamine echocardiographywas significantly better (P<0·00l). Thus dobutamineechocardiography is superior to exercise electrocardiographyfor diagnosis of coronary artery disease in hypertensive patients.     

Alterations in angina threshold with nifedipine during pacing induced angina

Changes in coronary haemodynamics and angina threshold were determined during atrial pacing in 11 patients with fixed obstructive coronary artery disease with effort angina before and after the administration of 20 mg of oral nifedipine. Coronary vascular resistance decreased at resting and at "subangina" heart rates but not at "angina" rates. Primary coronary vasodilatation with nifedipine was also suggested by higher coronary sinus oxygen content whether at rest or at subangina or angina heart rates. After nifedipine angina occurred at a lower double product and lower myocardial oxygen consumption. These findings suggest that nifedipine is a coronary vasodilator, but angina can occur at a lower angina threshold in some patients with obstructive coronary artery disease.     

Alterations in angina threshold with nifedipine during pacing induced angina.

Changes in coronary haemodynamics and angina threshold were determined during atrial pacing in 11 patients with fixed obstructive coronary artery disease with effort angina before and after the administration of 20 mg of oral nifedipine. Coronary vascular resistance decreased at resting and at "subangina" heart rates but not at "angina" rates. Primary coronary vasodilatation with nifedipine was also suggested by higher coronary sinus oxygen content whether at rest or at subangina or angina heart rates. After nifedipine angina occurred at a lower double product and lower myocardial oxygen consumption. These findings suggest that nifedipine is a coronary vasodilator, but angina can occur at a lower angina threshold in some patients with obstructive coronary artery disease.     

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.     

Coronary reserve, extent of coronary disease, recurrent angina and ECG changes during pain in the in-hospital prognosis of acute coronary syndromes

The prognostic value of recurrent angina, severity of coronarydisease, ECG changes during pain and coronary reserve (ischaemicthreshold measured by atrial pacing: heart rate with ST segmentshift = 1 mm), was evaluated in 383 consecutive patients withacute coronary syndromes. Univariate analysis showed a significantrelationship between occurrence of complications (death, infarctionor coronary surgery) and number of anginal episodes, extentof coronary disease, ischaemic threshold and ST depression withpain. A multivariate analysis indicated that the first threeparameters were the main independent predictors. Coronary reservewas reduced (threshold 150 beats. min^–1) in 83% of patientswho had a myocardial infarction (40), in 91% of those who died(11), in 87% of those who underwent coronary surgery (52) andin 47% of uncomplicated cases (301). Also, a low ischaemic thresholdwas associated with a larger number of anginal episodes thana high threshold ( 130 beats. min^–1, 6.1 ± 5.6vs > 150 beats. min^–1, 2.9± 4.1, P<0.0001),and in complicated patients with one-, two- or three-vesseldisease ischaemic threshold (137.3± 21.2, 133.3 ±18.9, and 135.1 ± 21.2 beats. min^–1, respectively)was lower than in the uncomplicated ones (153.4±20.1,P < 0.005; 148.2± 19.1 P < 0.005; and 139.2 ±23.0 ns, beats, min^–1). A threshold <150 beats. min^–1and ECG changes during pain identified the subset with the highestrisk for complications (59/137, 45%), whereas a threshold >150 beats. Min^–1 and absence of pain or ECG changes duringpain identified those with the lowest risk (5/109, 5%, p <0.001). Thus, our findings document the prognostic significance of coronaryreserve for in-hospital complications in patients with acutecoronary syndromes and confirm the prognostic value of previouslyknown risk markers. They also indicate that some of them maybe significantly influenced by the status of coronary reserve.     

The prognostic significance of post-infarction angina pectoris and the effect of verapamil on the incidence of angina pectoris and prognosis

The prognostic sign of angina pectoris and the effect of interventionwith verapamil on the incidence of angina pectoris were studiedin patients recovering from myocardial infarction and includedin the Danish Verapamil Infarction Trial II. During the secondweek after admission patients were double-blindly randomizedto treatment with verapamil 360 mg. day^–1 or placebo.Treatment was continued for up to 18 months. At discharge anginapectoris was reported in 11% of 869 patients randomized to verapamiland in 12% of 888 randomized to placebo (ns). One month afterdischarge a significantly increase in the prevalance of anginapectoris was reported in both the verapamil (33%) (P<0·001)and the placebo groups (39%) (P <0·001). The one monthprevalence of angina pectoris (P=0·03) and the 18 monthsoverall incidence of angina pectoris (P= 0·002) wereboth .sigificant lower in the verapamil group compared withplacebo. Stable angina pectoris during the first month of follow-upwas a significant predictor of major events (i.e. death or reinfarction)(hazard ratio = 1·45; 95% confidence limits: 1·101·89). As verapamil significantly reduced the incidenceof angina pectoris during daily activities, and thereby thenumber of patients at high risk, the beneficial effect of verapamilin reducing major events in patients recovering from myocardialinfarction is likely to be due to abolishing myocardial ischaemia.