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Background: The aim of this study was to evaluate enoximone echocardiography (EE) for the identification of residual myocardial viability in postinfarction patients. Findings obtained during EE were compared with those acquired by myocardial uptake of fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) and functional follow-up results. Methods: Twenty-five patients underwent EE and PET 18F-FDG studies. An asynergic segment was considered as having contractile enhancement when the wall motion score decreased by >= 1 grade during EE and was defined as viable if 18F-FDG uptake score was >= 2 grade on PET. Results: Of 293 dysfunctional segments at baseline, 139 (47%) were viable by PET criteria; 117 (40%) had contractile enhancement induced by enoximone (P = 0.07). Agreement between EE and PET was found in 75% of involved segments (K = 0.46, P < 0.001). The majority of discrepancies (65%, P < 0.01) were mainly due to discordant segments in which PET revealed evidence of 18F-FDG uptake but EE showed no change in wall motion. In 179 revascularized segments, negative predictive value for functional recovery of both tests reached the same value (89% for both), whereas positive predictive value was 82% for EE and 68% for PET, respectively (P < 0.05). Sensitivity was 85% for EE and 88% for PET (P = ns); specificity was 87% and 70%, respectively (P < 0.01). Conclusions: EE yields a fair concordance with PET study. Compared with PET, despite a similar negative accuracy, EE shows a greater specificity for prediction of function recovery after revascularization. (Echocardiography 2010;27:544-551). RI Balbarini, Alberto/G-8753-2011

Little information is available on the long-term evolution of left ventricular function of medically treated patients with coronary artery disease and gross limitation of coronary flow reserve. The aim of this study was to assess the long-term evolution of effort tolerance and left ventricular function and their relation to the control of ischemic events in patients with coronary artery disease and prolonged inducible exercise-induced myocardial dysfunction who either declined or were ineligible for cardiac revascularization.

We report a complication observed in a 77-year-old man admitted to another hospital for "de novo" angina, in which coronary angiography showed a proximal 65% stenosis of the left anterior descending artery. The patient was medically stabilized, but one month later he developed unstable angina that was not controlled by heparin, nitrate and calcium antagonist infusions. Therefore, he was started on ReoPro (0.25 mg/kg bolus and 10 micrograms/min infusion) but because of persisting symptoms, he was transferred to our unit for urgent PTCA. Angioplasty plus stenting was successful and angina disappeared. The ReoPro infusion was stopped (6 hours after it had been started) for mild oral bleeding. Blood analysis was normal (including platelet count) except for the activated partial thromboplastin (PTT) and prothrombin (PT) time, which exceeded the laboratory limits of determination. Consequently, heparin infusion was also stopped. Eight hours after PTCA, he suddenly developed hypotension, bradycardia and loss of consciousness. The echocardiogram revealed a large pericardial effusion with diastolic collapse of the right cardiac chambers. The patient was treated with volume expanders, plasma and platelet units in an attempt to reestablish a normal hemodynamic pattern and normal platelet function. Elective pericardiocentesis was performed 24 hour later, with drainage of 800 ml of hematic effusion. Severe hemorrhagic complication was induced by ReoPro despite a normal platelet count. This was successfully counteracted with plasma and platelet infusion.

Palpitation is an unpleasant awareness of an abnormal beating of the heart. This symptom may be brought on by a variety of cardiac disorders, such as cardiomyopathy, valvular heart disease, and coronary artery disease, but the most common cause is primary cardiac arrhythmias. Several noncardiac disorders may also cause palpitations, and in this case are an effect of the disease upon cardiac rhythm. Palpitations occur frequently in women at all ages, especially during the luteal phase of the menstrual cycle, during pregnancy, and during the perimenopausal period. Palpitations occurring at young age and associated with fast heart rate are frequently due to Wolff-Parkinson-White syndrome or other forms of re-entrant tachycardia, and may require catheter ablation. A correlation between ovarian hormones and occurrence of paroxysmal supraventricular tachycardia has recently been reported in female patients with normal menstrual cycles; palpitations are frequently reported in cases of mitral valve prolapse, whereas episodes of paroxysmal supraventricular tachycardia reported during pregnancy may be due to mechanical stimuli or to a suggested arrhythmogenic effect of pregnancy. Palpitations during the perimenopausal period are usually benign and seem to be related to the increased sympathetic activity caused by the menopause. Although the vast majority of palpitations are benign and need not be treated, an electrophysiological study is indicated for those patients who have a documented episode of palpitation associated with syncope or with a pulse that is inappropriately rapid during symptoms. The treatment of palpitations due to cardiac arrhythmias is dependent upon the kind of arrhythmia detected during either invasive or noninvasive electrophysiological studies.

The assessment of residual myocardial viability in infarcted areas is relevant for subsequent management and prognosis but requires expensive technology. To evaluate the possibility that simple, easily obtainable clinical markers may detect the presence of within-infarct viable tissue, the significance of exercise-induced ST elevation occurring in leads exploring the area of a recent Q wave myocardial infarction was assessed. Twenty-five patients with recent (< 6 months) myocardial infarction were studied. All had angiographically documented coronary artery disease, diagnostic Q waves (n = 24) or negative T waves (n = 25) on the rest 12-lead electrocardiogram and exhibited during exercise greater-than-or-equal-to 1.5 mm ST segment elevation (n = 17) or isolated T wave pseudonormalization (n = 8) in the infarct-related leads. ST-T wave changes were reproduced in all patients during thallium-201 exercise myocardial scintigraphy. A fixed perfusion defect was observed in 24 of the 25 patients. A reversible defect was seen in 16 (94%) of 17 patients who exhibited transient ST elevation during exercise but in only 4 (50%) of the 8 patients who had only T wave pseudonormalization. In conclusion, in patients with recent myocardial infarction, analysis of simple ST segment variables obtained during exercise testing may allow a first-line discrimination of those who may potentially benefit from a revascularization procedure.

Background: We investigated the possibility that transient coronary slow-flow as assessed during coronary angiography in patients with cardiac syndrome X may impair myocardial perfusion and the effects of this phenomenon on long-term prognosis. Methods: From 50 consecutive patients with cardiac syndrome X, we prospectively recruited 16 who exhibited coronary slow-flow during angiography. The remaining 34 patients served as controls. The slow-flow phenomenon was invariably worsened by nitrates and reversed by papaverine. During slow-flow, a dose of 99m-Tc-Methoxy-isobutyl-isonitrile (MIBI) was injected in 12 patients and SPECT imaging performed 1 h later. The perfusion study was repeated after 2 days at rest and, in 9 patients, at peak exercise after 10 +/- 4 days. Patients were then regularly followed-up. Results: All 12 patients had a significant MIBI defect in the regions served by the coronary artery that showed slow-flow just prior MIBI injection. After exercise, MIBI tomograms revealed a perfusion defect in 5 out of the 9 patients who underwent stress scanning. At 14 +/- 2 years follow-up, 1 patient with slow-flow had died and 4 developed significant coronary artery disease (CAD), while all patients of the control group were alive and none had developed significant CAD. Conclusions: These results show that the slow-flow phenomenon might be the cause of transient myocardial underperfusion in patients with angina and normal coronary arteries. Apparently, this phenomenon is associated with a worse cardiac prognosis. Therefore, patients with coronary slow-flow should be carefully followed-up. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

OBJECTIVES We assessed the short- and long-term clinical and angiographic outcome of nonocclusive unstented dissection after percutaneous transluminal coronary angioplasty (PTCA) and its correlation with restenosis. BACKGROUND The use of stents has dramatically increased both the number and the cost of coronary revascularization procedures. However, this technique is not completely risk free, and its benefits have not been fully demonstrated in uncomplicated dissections. METHODS We studied 129 consecutive patients with 49 nonocclusive dissections after PTCA (grades A to D of National Heart, Lung, and Blood Institute classification) and good distal Asw (TIMI [Thrombolysis in Myocatdial Infarction] flow grade 3). All patients underwent coronary angiography at 24 h and at six months past-PTCA. Clinical status was assessed every three months in the outpatient clinic. Study subjects were matched with 60 other patients in whom stenting was performed for the presence of dissection. RESULTS In the former group, all but two patients (with type E dissection, which evolved to coronary occlusion and myocardial infarction) improved their dissection score during follow-up: at six months only 18 dissections were still angiographically visible, and no clinical adverse events were recorded. In the dissected vessels, the restenosis rate was significantly lower than in those without dissection (12% vs. 44%, p < 0.001); in the stented vessels, the restenosis rate was 25% (15/60). CONCLUSIONS In the presence of TIMI flow grade 3, coronary dissection is associated with a favorable outcome and predicts a low restenosis rate. These results caution against the indiscriminate use of intravascular prostheses in the event of nonocclusive coronary dissection. (C) 1999 by the American College of Cardiology.

Objectives. This study sought to investigate whether residual viability of infarcted myocardium may play a role in the pathogenesis of exercise-induced ventricular arrhythmias. Background. We previously showed that transient ischemia within partially infarcted areas often precipitates ventricular arrhythmias during exercise that are consistently obliterated by intravenous nitrates. Methods. We studied 60 patients with chronic stable angina and a previous myocardial infarction, All underwent at least two consecutive exercise stress tests, coronary angiography and stress/rest myocardial perfusion tomography by Tc-99m 2-methoxy isobutyl isonitrile (MIBI). In the last 26 consecutive patients, residual viability was assessed by single-photon emission computed tomography (SPECT) using fluorine (F)-18 fluorodeoxyglucose. Perfusion and metabolic data were evaluated qualitatively by three independent observers in blinded manner, Results. With exercise, 30 patients (group A) consistently developed ventricular arrhythmias (>10 ventricular ectopic beats/min, couplets, nonsustained ventricular tachycardia); the remaining 30 patients (group B) did not, The severity of coronary artery disease (Gensini score) was similar in the two groups. Posterercise SPECT shun ed partial reperfusion of an infarcted area in 28 of 30 patients of group A but in only 9 of 30 of group B (p < 0.0001). Uptake of F-18 fluorodeoxyglucose was observed within the infarcted zone in 10 of 13 and 1 of 13 patients in groups A and B, respectively (p = 0.0003). Conclusions. In patients with myocardial infarction, exercise-induced ventricular arrhythmias appear to be triggered by transient ischemia occurring within a partially necrotic area containing large amounts of viable myocardium. Therefore, occurrence of arrhythmias during exercise may represent a clue to the presence of residual viability within a previously infarcted area. RI Lucignani, Giovanni/C-6773-2008

Thirteen hypertensive patients with microvascular angina were studied before and after receiving oral L-arginine (4 weeks, 2 g, 3 times daily). L-arginine significantly improved angina class, systolic blood pressure at rest, and quality of life. Maximal forearm blood flow, plasma L-arginine, L-arginine:asymmetric dimethyl arginine ratio, and cyclic guanylate monophosphate increased significantly after treatment. In medically treated hypertensive patients with microvascular angina, oral L-arginine may represent a useful therapeutic option. (C) 2004 by Excerpta Medica, Inc.

Diazepam (DZP) is commonly used in treatment of patients with acute ischemic syndromes to allay anxiety, but benzodiazepines reduce myocardial contractility and increase myocardial blood flow. To investigate the antiischemic effect of DZP, we studied 13 patients with a positive exercise test and angiographically documented coronary artery disease. All patients were submitted to a randomized, placebo-controlled trial using 0.9% NaCl infusion as placebo and intravenous (i.v.) diazepam (0.1 mg/kg in 20 min). Exercise tests performed immediately after the infusions showed that as compared with placebo, DZP significantly prolonged time to 1-mm ST-segment depression (557 +/- 198 vs. 428 +/- 226 s, p < 0.0001) and total exercise duration (624 +/- 177 vs. 561 +/- 188 s, p < 0.007). Rate-pressure product (RPP) at 1-mm ST-segment depression was not significantly different with the two treatments. DZP significantly delays onset of exercise-induced myocardial ischemia in patients with coronary artery disease. Because RPP at onset of ischemia was similar to that recorded with placebo despite greater levels of external workload, the antiischemic action of DZP appears to be mediated, at least partially, by a reduction in myocardial oxygen consumption.

In patients with myocardial infarction, the distinction between reversible and irreversible ventricular dysfunction has important clinical implications since dysfunctional but viable myocardium will resume contraction following revascularization. Various methods have been developed for the identification of potentially reversible myocardial dysfunction. Thallium reinjection, immediately after stress-redistribution imaging, may provide evidence of myocardial viability by demonstrating thallium uptake in regions with apparently 'irreversible' defects. Hypoperfused, hypocontractile segments may recover function after revascularization, when exhibiting increased 18F-fluoro-deoxy-glucose uptake on positron emission tomography. Improved contractile function by selective beta 1 adrenergic stimulation with low dose dobutamine may also indicate the presence of viable tissue and predict subsequent improvement upon restoration of adequate flow. Finally, exercise-induced ST segment elevation on leads exploring a recent myocardial infarction has also been shown to indicate the presence of viable, potentially salvageable tissue. We discuss here these and several other methods that have been proposed for the detection of residual myocardial viability. Their advantages, limitations, and relevance to clinical problems are also discussed.

Although in experimental models of coronary occlusion diltiazem administration has been shown to reduce the degree of stunning and of reperfusion injury, the majority of clinical trials has failed to demonstrate significant benefits. The aim of this study was to evaluate the effect of diltiazem, administered before coronary reperfusion, on infarct size, residual myocardial viability and recovery of left ventricular function.We studied 90 patients admitted within 3 hours of the onset of symptoms of acute myocardial infarction. They were immediately randomized to either intravenous diltiazem (10 mg bolus + 10 mg/hour for 3 days) (group 1, n = 43) or placebo (group 2, n = 47) and subsequently treated with recombinant tissue-type plasminogen activator. All underwent serial echocardiograms upon admission, 4 days post-admission during low-dose dobutamine stress echo, at discharge and after 6 months. We calculated the dysfunction score (1 = hypokinesia, 2 = akinesia, 3 = dyskinesia) on admission and its percent reduction after dobutamine (viability) and at follow-up (recovery). The 12-lead electrocardiograms were continuously monitored for 3 days and coronary angioplasty was performed whenever the residual stenosis was60%.Upon admission, there were no differences in age, sex, infarct location and size, degree of ST-segment elevation, time from onset of symptoms and dysfunction score. Creatine kinase peaked early in 70% of patients in both groups; the incidences of recurrent ischemia, infarct-related vessel patency and the need for coronary angioplasty were also similar. The creatine kinase peak was significantly higher in group 2 (2931 +/- 2456 vs 1726 +/- 1004 IU/l, p0.05). Conversely, in group 1 the residual viability was significantly higher (51 +/- 23 vs 36 +/- 30% improvement in dysfunction score, p0.05) and the early recovery of regional function was significantly greater (35 +/- 34 vs 18 +/- 22% at discharge, p0.05). On the other hand, the delayed recovery was not significantly different (15 +/- 29 vs 21 +/- 32% from the time of discharge to 6 months of follow-up).Intravenous diltiazem, started before coronary reperfusion, has beneficial effects on the infarct size, residual viability and recovery of regional function. If confirmed by larger trials, these preliminary results suggest the use of diltiazem as adjunctive therapy in patients with acute myocardial infarction and undergoing reperfusion.

Sixteen postmenopausal women underwent electrophysiologic study before and 20 minutes after the administration of sublingual estradiol 17beta or placebo. Estradiol 17beta significantly affected electrophysiologic parameters, thereby suggesting its role in the development of palpitations in women.

Background —The possibility that enoximone, a nonglycoside, noncatechol, positive inotropic agent, in combination with 2-dimensional echocardiography may predict recovery of myocardial dysfunction after revascularization has not been yet evaluated. Methods and Results —Forty-five patients with chronic coronary artery disease and left ventricular dysfunction underwent dobutamine (DE, 5 to 10 μg · kg −1 · min −1 ) and enoximone (EE, 1.5 mg/kg, over 10 minutes) echocardiography. Myocardial wall motion was scored from 1 (normal) to 4 (dyskinesia): an asynergic segment was considered to have contractile enhancement when the score decreased by ≥1 grade. Of 478 asynergic segments, 216 (45%) exhibited functional recovery after revascularization. Dobutamine- and enoximone-induced contractile enhancement was observed in 41% and 46% of segments, respectively. Compared with DE, EE had higher sensitivity (88% versus 79%, P P P Conclusions —Enoximone echocardiography provides a novel and reliable approach for the prediction of functional recovery after revascularization. Compared with dobutamine echocardiography, the test yields higher sensitivity and induces lesser hemodynamic alterations.

Aims We investigated the ability of T-wave pseudonormalization and ST-segment elevation, which are demonstrated in infarct-related leads during submaximal exercise testing, to predict late recovery of contractile function. Methods We studied 88 consecutive patients (73 males, mean age 59+/-8 years) with anterior infarction, persistent T-wave inversion and a documented lesion of the proximal segment of the left anterior descending coronary artery. They all underwent 2D-echocardiography on admission, 4 weeks as well as 6 months after myocardial infarction to evaluate the dysfunction score and the ejection fraction. Submaximal (75% of maximal predicted heart rate) exercise testing was performed in 80 patients 2 weeks after myocardial infarction following discontinuation of treatment. Results During exercise testing, 59 of the 88 patients showing negative T-waves on the resting electrocardiogram exhibited pseudonormalization (group A) in at least three adjacent precordial leads, whilst 29 (group B) did not. Patients of group A more frequently exhibited an early creatine kinase peak (41% vs 24%, P

In previously thrombolysed patients, we analysed residual myocardial viability using the PET-FDG technique and correlated its presence and extent to the angiographic appearance of the infarct-related vessel and left ventricular function. Thirty-six patients who had undergone intravenous thrombolysis for acute myocardial infarction 4.8 +/- 7.2 months previously were studied. Coronary angiography, left ventriculography, and assessment of myocardial perfusion and metabolism were all performed within 1 week. All patients exhibited perfusion defects consistent with the clinically identified myocardial infarction site. Residual viability, as assessed by the PET-FDG technique, was present in 53% of cases. The infarct-related coronary artery was patent in 19 (53%) patients (TIMI grade 3, 79%); of the remaining 17 with occluded infarct-related arteries, 11 had collaterals to the infarct area. Significant FDG uptake was observed in 63% of patients with a patent infarct-related artery and in 41% of those with an occluded infarct-related artery. The same study protocol was adopted in a control group of 30 patients with myocardial infarction who did not receive thrombolysis. The number of infarct-related patent vessels was significantly lower in these patients (30 vs 53%) (TIMI grade 3, 56%), but the overall percentage of PET viability was again 53%. Qualitative analysis of the regional perfusion pattern showed that the magnitude and severity of the perfusion defect was similar in the two groups, regardless of the presence or absence of FDG uptake. Global left ventricular function was also similar in the two groups. However, regional wall motion was significantly better in the thrombolysed patients with a patent infarct-related artery than in those who had not received thrombolysis and whose culprit vessel was also patent. In conclusion, the results of our study support the notion that early recanalization of the infarct-related artery is critical for preserving left ventricular function. Although the number of patent infarct-related coronary arteries is greater and left ventricular function is better in successfully thrombolysed patients, the regional metabolic pattern does not apparently correlate with the patency of the infarct-related artery. This suggests that, in 'chronic' myocardial infarction, residual tissue viability as assessed by fluorodeoxyglucose uptake does not necessarily correlate with coronary recanalization. RI Lucignani, Giovanni/C-6773-2008

Background Controversial evidence exists as to whether thrombolytic therapy reduces the incidence of left ventricular thrombus in acute myocardial infarction and, if so, how this relates to successful reperfusion. Methods Four hundred and eighteen consecutive patients underwent echocardiography and coronary angiography within 3 weeks of an acute myocardial infarction. A dyssynergic score was calculated by analysing regional wall motion in 18 left ventricular segments. The infarct-related artery was considered patent if TIMI grade 2 or 3 flow and less than 90% stenosis were present. Retrograde perfusion by Rentrop's grade 2 or 3 collaterals was considered significant. Results Large anterior myocardial infarctions were associated with the highest prevalence (39%) of left ventricular thrombosis. Thrombus was also very frequent if the left anterior descending coronary artery was occluded and no collaterals to the infarct area were seen (75%). Anticoagulant therapy reduced the prevalence of left ventricular thrombus, regardless of whether the infarct-related vessel was patent or not. Conversely, in patients undergoing thrombolysis the incidence of left ventricular thrombosis was lower when the left anterior descending coronary artery was patent, and especially when an early creatine kinase peak, suggestive of reperfusion, was recorded (7%). Finally, the presence of left ventricular thrombosis was inversely related to the asynergy score. Conclusion These observations suggest that the presence of left ventricular thrombus is related to the extent of myocardial damage. Thrombolytic therapy reduces thrombus probably by salvaging myocardium at risk. (Eur Heart J 1996; 17: 421–428)

Objectives. In a prospective study we evaluated whether late recanalization of the left anterior descending coronary artery (LAD) affects ventricular volume and function after anterior myocardial infarction. Background. Persistent coronary occlusion after anterior myocardial infarction leads to ventricular dilation and heart failure. Methods. We studied 73 consecutive patients with acute anterior myocardial infarction as a first cardiac event; all had an isolated lesion or occlusion of the proximal LAD. Six patients died before hospital discharge. The 67 survivors were classified into two groups: group I (patent LAD and good distal flow, n = 40) and group II (LAD occlusion or subocclusion, n = 27). The 20 patients in group I who had significant residual stenosis and all patients in group II underwent elective percutaneous transluminal coronary angioplasty (PTCA) within 18 days of myocardial infarction. The procedure was successful in 17 patients in group I (group IB) and in 16 patients in group n (group IIA): in the remaining 11 patients of group II, patency could not be reestablished (group IIB). Left ventricular volumes, ejection fraction and a dysfunction score were measured by echocardiography on admission, before PTCA, at discharge and after 3 and 6 months. Results. Although cumulative ST segment elevation was similar in groups I and II, ejection fraction and dysfunction score were significantly worse in group II. However, ventricular function and volumes progressively improved in group IIA, whereas group IIB exhibited progressive deterioration of function (dysfunction score [mean +/- SD] increased from 21 +/- 6 to 25 +/- 8, p < 0.05; ejection fraction decreased from 43 +/- 10% to 37 +/- 11%, p < 0.05); and end-systolic volume increased from 34 +/- 10 to 72 +/- 28 ml/m(2), p < 0.05). Patients in group IIB also had worse effort tolerance, higher heart rate at rest, lower blood pressure and significantly greater prevalence of chronic heart failure. Conclusions. Delayed PTCA of an occluded LAD can frequently restore vessel patency. Success appears to be associated with better ventricular function and a lack of chronic dilation. Large randomized studies are warranted to evaluate the effect of delayed PTCA on late mortality.

Objectives. We evaluated the sensitivity and specificity of exercise induced ST segment elevation for the detection of residual myocardial viability. Background. Assessment of residual viability after myocardial infarction is relevant for establishing indication for revascularization. We have previously shown that exercise-induced ST segment elevation is a marker of residual viability. Methods. We studied 34 patients,vith a previous Q wave myocardial infarction (anterior in 21, inferior in 13) of whom 18 (group A) had exercise-induced ST segment elevation in more than one lead (mean [+/-SD] 1.8 +/- 0.9 mm, range 1 to 4) and 16 (group B) did not. All patients underwent rest technetium-99m methoxyisobutyl isonitrile single-photon emission computed tomography (SPECT), fluorine-18 (F-18) fluorodeoxyglucose positron emission tomography and coronary angiography. The time elapsed between the infarction and the viability study was 72 +/- 108 days (range 15 to 400) in group A and 516 +/- 545 days (range 14 to 1,800) in group B. Results. The presence and site of previous infarction were confirmed by SPECT studies in all 34 patients. Uptake of F-18 fluorodeoxyglucose within the infarcted area was present in 18 of 18 patients in group A but in only 9 (56%) of 16 in group B (p < 0.01). In patients with an anterior infarction, the sensitivity, specificity and predictive accuracy of exercise-induced ST segment elevation for detection of residual viability were 82%, 100% and 86%, respectively (95% confidence intervals 46% to 83.5%, 59% to 100% and 55.6% to 87.1%, respectively). Conclusions. Exercise-induced ST segment elevation in infarct-related leads has a high specificity and acceptable sensitivity for detection of residual viability within the infarcted area. RI Lucignani, Giovanni/C-6773-2008

The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post-PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82%, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post-PTCA (-31.54 ± 10.65%) and stenotic segments (-23.08 ± 11.88%) than in the reference and remote segments (respectively, -14.88 + 7.63% and - 18.67 + 8.37%, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium-mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64)

The role of collaterals in influencing postischemic recovery after exercise testing has not been investigated previously. We studied 54 patients (mean age 59 +/- 6 years) with effort-induced angina and documented coronary disease who underwent exercise testing and thallium-201 myocardial scintigraphy. On angiography, 30 patients (group A) exhibited visible collaterals (grade 2 to 3, Cohen and Rentrop classification) perfusing the ischemic zone, whereas the other 24 (group B) did not. Patients with collaterals had more severe coronary artery disease (Gensini score 46.9 +/- 16 vs 28.6 +/- 18; p less than 0.001) and more severe impairment of coronary flow reserve (time and rate-pressure product to 1 mm ST segment depression 3.5 +/- 0.8 vs 4.8 +/- 0.6 minutes, p less than 0.01; 14,189 +/- 2451 vs 16,081 +/- 2215 beats/min x mm Hg, p less than 0.04, respectively). However, in these patients the ECG returned to baseline more rapidly after exercise (5.5 +/- 1.6 vs 11.7 +/- 3.3 minutes; p less than 0.001). Therefore, although collaterals do not apparently prevent or delay the development of exercise-induced ischemia, they can limit its duration by allowing a faster recovery.

In patients with coronary artery disease, electrocardiographic signs of left atrial enlargement (LAE-negative P wave deflection greater than or equal to 1 mm2 in lead V1) are associated with increased left ventricular end diastolic pressure (LVEDP). We investigated the possibility that transient LAE could represent an additional criterion for diagnosing myocardial ischemia during exercise testing (EST). We studied 48 consecutive patients with chronic stable angina, positive EST and 201 Tl scintigraphy, and angiographically proven CAD; 200 other consecutive patients with atypical chest pain and normal stress/rest 201 Tl scintigraphy served as controls. During EST, transient LAE developed in 34/48 patients with CAD but in only 1/200 controls (p less than 0.001). When present, LAE preceded ST changes (6.1 +/- 1 min vs 8.2 +/- 2 min) and recovered earlier (4.7 +/- 4 min vs 5.8 +/- 3 min). The prevalence of 2-3 vessel CAD was significantly higher in patients with EST-induced LAE (54% vs 34%, p less than 0.05). In conclusion, transient ECG signs of LAE during EST represent a highly specific sign of reversible ischemia and are frequently associated with multivessel CAD. Although less sensitive than classical ST criteria, this sign may prove useful in patients exhibiting equivocal ST changes and in the presence of ventricular conduction disturbances.

In patients with ischemic heart disease and arrhythmias, selection of antiarrhythmic treatment is often difficult as it is hard to separate "primary" from ischemic arrhythmias. We studied 20 patients with ischemic heart disease, who developed ventricular arrhythmias consistently during exercise test. Exercise test was performed twice during infusion of placebo and then during intravenous administration of nitroglycerin, titrated to reduce systolic blood pressure by 10 mmHg. Exercise duration was 7.8 +/- 1.7 and 7.9 +/- 1.5 min, in the 2 placebo tests (NS). Angina developed in 5 patients and ischemic ST changes in 10. With nitroglycerin exercise duration increased to 8.4 +/- 20 min (p less than 0.05), diagnostic ST segment depression was observed in 2 patients and only 1 had angina. In all 20 patients, ventricular arrhythmias were consistently present during both tests on placebo, that were markedly reduced by nitroglycerin. In fact, ventricular ectopic beats were 455 (mean 35.8 +/- 16.8) and 418 (mean 34.4 +/- 11.1) in the 2 exercise tests with placebo, and 11 during nitroglycerin infusion (mean 0.6 +/- 0.1; p less than 0.001). Couplets were 28 and 29 during placebo (NS) and 0 during nitroglycerin (p less than 0.001). Ventricular tachycardia was present in 6 and 8 patients during placebo but in none during nitroglycerin (p less than 0.001). Reduction of exercise-induced arrhythmias was maintained during chronic treatment with oral vasodilators. Prevention of exercise-related arrhythmias by nitroglycerin infusion appears a good indicator of their ischemic origin and may provide valuable information for long-term profilaxis with oral vasodilators, then avoiding the use of antiarrhythmic agents and their potential side effects.