Computationally inexpensive methods for intra-cardiac atrial bipolar electrogram compression.

AIM: This paper reports studies of mathematical algorithms for intra-cardiac atrial bipolar electrogram compression suitable with implementation on implantable devices. PATIENTS AND METHODS: Bipolar intra-cardiac electrograms (IEGMs) of high right atrium were obtained from 20 patients who underwent electrophysiological studies for arrhythmias. Four thousand seven hundred and eighty-two seconds of IEGM were collected and divided into three rhythm groups: sinus rhythm (SR), atrial fibrillation (AF) and atrial flutter (AFL). Since mathematical algorithms suitable for use with implantable devices demand low computational cost, we employed piecemeal linear approximation methods (ZOP--Zero Order Prediction and SAPA--Scan Along Polygonal Approximation), and beat detection method (Peak) both or which need small numbers of operations to perform electrogram compression. Compression ratio (CR) and percent root mean square difference (PRD) were used to compare the three methods, with statistical analyses performed using paired t-test. RESULTS AND CONCLUSION: The best performance was obtained using the Peak method which reaches an average CR of 10.6 in the case of SR group, 2.8 for AF, and 3.6 for AFL groups, respectively, while PRD lies below 2% for SR and AFL groups and 6% for the AF group. Results show that, for bipolar electrograms, the Peak method reaches statistically significant better performance (P<0.001) in all cases except for Peak vs SAPA applied to AF (P=0.2). The number of operations necessary to compress the data indicate that time consumption can be reduced to be suitable for real time compression in implantable devices. The Peak method, which was assumed to receive the instant of occurrence of each recognized beat, from the hardware of the device, requires fewer operations than ZOP and SAPA. Increasing the length of electrograms recorded in pacemakers will enhance the amount of information provided by the implantable device, allowing more detailed characterization of the intra-cardiac activity and leading to new perspectives in arrhythmia diagnosis and therapy.

Complete or incomplete percutaneous coronary revascularization in patients with unstable angina in stent era: Are early and one-year results different?

The aim of our study was to evaluate the impact of a strategy of incomplete revascularization by PTCA, with or without stent implantation, on clinical outcome of 208 consecutive patients (171 men) with unstable angina and multivessel coronary artery disease. Mean age of the group was 63.8 +/- 10.3 years (range, 31-91). Complete and incomplete revascularization was achieved in 49 and 159 patients, respectively. A total of 226 stents were implanted in 172 patients (1.31 +/- 0.65 stent per patient), equally distributed between the two groups. Left ventricular ejection fraction < 40% and total chronic coronary occlusions were significantly more frequent in patients with incomplete revascularization than in those with complete (P = 0.014 and 0.001, respectively). In-hospital MACE occurred in 10% and 7.5% of patients with complete and incomplete revascularization, respectively (P = NS). By multivariate analysis, multiple stent implantation (OR, 5.44; 95% CI, 1.21-24.3), presence of thrombus in the treated lesion (OR, 6.3; 95% CI, 1.53-25.9), Braunwald class III (OR, 4.74; 95% CI, 1.08-20.8), and ad hoc PTCA (OR 4.51; 95% CI, 1.11-18.3) were significantly related to in-hospital outcome. At 1-year follow-up, 11.3% and 11.5% of patients with complete and incomplete revascularization, respectively, had MACE. In all patients, diabetes (OR, 3.40; 95% CI, 1.09-10.58) and presence of thrombus in the treated lesion (OR, 3.48; 95% CI, 1.12-10.84) were significant predictors of 1-year outcome by multivariate analysis. These results indicate that the strategy of incomplete revascularization in unstable angina patients with multivessel coronary disease does not expose them to a higher risk of death or other major ischemic events in comparison to those undergoing complete revascularization.

Beneficial effects of diltiazem during myocardial reperfusion: a randomized trial in acute myocardial infarction.

BACKGROUND: 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. METHODS: 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 was > 60%. RESULTS: 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, p < 0.05). Conversely, in group 1 the residual viability was significantly higher (51 +/- 23 vs 36 +/- 30% improvement in dysfunction score, p < 0.05) and the early recovery of regional function was significantly greater (35 +/- 34 vs 18 +/- 22% at discharge, p < 0.05). 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). CONCLUSIONS: 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.

[Inflammation and acute coronary syndromes]. / Inflamación y síndrome coronario agudo.

A great variety of stimuli, such as free radicals, oxidized LDL or some bacteria or virus infections, can act upon the vascular surface and lead to the development of an acute inflammatory reaction. There is more and more evidence supporting the hypothesis that the mechanism responsible for the transformation of a non-complicated atherosclerotic lesion into an hemorrhagic and ulcerated lesion, with the subsequent acute and unstable clinical status, is due to the onset of an inflammatory reaction. Many studies have tried to investigate the presence of any systemic marker able to predict the prognosis of patients at risk from developing acute events, and to distinguish them from those in stable status. The increase of the levels of C-reactive-protein has been related to the development of acute coronary syndromes, though often the results obtained in the different studies have had a quite poor prognostic value when applied to the general population. The lack of direct association between the increase of the levels of C-reactive-protein and Troponin I seems to rule out the possibility that the inflammatory stimulus might be the consequence of an irreversible injury, even though there is no doubt that severe ischemia is likely to play an active role in this sense.

Triglycerides impair postischemic recovery in isolated hearts: roles of endothelin-1 and trimetazidine.

There is growing evidence that hypertriglyceridemia exacerbates ischemic injury. We tested the hypothesis that triglycerides impair myocardial recovery from low-flow ischemia in an ex vivo model and that such an effect is related to endothelin-1. Hyperglycemic (glucose concentration = 12 mmol/l) and hyperinsulinemic (insulin concentration = 1.2 micromol/l) isolated rat hearts were perfused with Krebs-Henseleit buffer (PO(2) = 670 mmHg, pH 7.4, 37 degrees C) added with increasing triglycerides (0, 1,000, 2,000, and 4,000 mg/dl, n = 6-9 rats/group). Hearts were exposed to 60 min of low-flow ischemia (10% of basal coronary flow), followed by 30 min of reperfusion. We found that increasing triglycerides impaired both the diastolic (P < 0.005) and systolic (P < 0.02) recovery. The release of endothelin-1 during reperfusion increased linearly with triglyceride concentration (P = 0.0009). Elevated triglycerides also increased the release of nitrite and nitrate (NO(x)), the end products of nitric oxide, up to 6 micromol/min. Trimetazidine (1 micromol) further increased NO(x) release, blunted endothelin-1 release, and protected myocardial function during recovery. We conclude that high triglyceride levels impair myocardial recovery after low-flow ischemia in association with endothelin-1 release. The endothelium-mediated effect of triglycerides on both contractile recovery and endothelin-1 release is prevented by 1 microM trimetazidine.

Time course and determinants of left ventricular function recovery after primary angioplasty in patients with acute myocardial infarction.

OBJECTIVES: We sought to evaluate the importance of time in relation to treatment, time course and determinants of recovery of left ventricular (LV) function in patients with acute myocardial infarction (AMI) undergoing primary percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Myocardial salvage has been shown to be dependent on the time elapsed from the onset of AMI to reperfusion. METHODS: Left ventricular function was evaluated at hospital admission, after angioplasty, at 24 h and 6 months by both echocardiography and angiography and at 1, 7, 30, 90 and 180 days by echocardiography in 101 consecutive patients. RESULTS: Patients were allocated to three groups according to interval between symptom onset and angioplasty: <2 h (group A), 2 to 4 h (group B) and >4 h (group C). Patients in groups A and B showed a progressive improvement of LV function between day 7 and day 90, which became statistically significant at day 30 (p < 0.01). No LV function changes were noted in group C patients. Thrombolysis In Myocardial Infarction (TIMI) flow grade <3 at 24 h was not associated with any significant change in LV volume and function during the six-month follow-up period. Restenosis, when associated with TIMI flow grade 3 in the infarct-related vessel, did not influence LV function. Flow grade <3 of the infarct-related artery was not associated with any improvement of cardiac events independently from the time to treatment at the initial procedure. CONCLUSIONS: Patients undergoing primary PTCA for AMI have a good recovery of LV function if TIMI flow grade 3 is restored within 4 h. Coronary angioplasty limits further remodeling of the LV in patients treated after 4 h.

Evidence for the involvement of phosphatidylinositol 3-kinase in fMLP-stimulated neutrophil adhesion to ICAM-1-transfected cells.

Phosphatidylinositol 3-kinase (PI-3K) controls important intracellular steps involved in inflammation, immunity, and cell growth. PI-3K also modulates leukocyte integrin adhesiveness. In this study we evaluated the role of PI-3K on neutrophil adhesion to intercellular adhesion molecule-1 (ICAM-1)-transfected cells. N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated neutrophil adhesion was inhibited by wortmannin and LY294002, two unrelated PI-3K inhibitors, whereas phorbol myristate acetate (PMA)-induced neutrophil adhesion was not inhibited by them. After fMLP stimulation, a rapid activation of AKT and ERK was observed. However, only activation of AKT was reversed by the PI-3K inhibitors. Neutrophil expression of the beta2-integrins Mac-1, lymphocyte function-associated antigen-1(LFA-1), and gp150.95 was not affected by wortmannin, nor was expression of the activation epitope recognized by MAB24. We conclude that (a) PI-3K is involved in fMLP-activated neutrophil adhesion to ICAM-1-transfected cells, (b) the mechanism involved is not mediated by the modulation of beta2-integrin expression or activation, and (c) another mechanism seems to involve the adhesion to ICAM-1 when a cellular system of adhesion is used.

Dobutamine stress echocardiography and the effects of trimetazidine on left ventricular dysfunction in patients with coronary artery disease.

Trimetazidine, a metabolic agent that is opening the way to a new class of 3-ketoacyl coenzymeA thiolase inhibitors, has been shown to improve exercise tolerance and increase the ischaemic threshold in patients with effort angina, both in monotherapy or in combination with other anti-anginal drugs. The aim of this study was to assess the effects of oral trimetazidine on the ischaemic threshold and left ventricular dysfunction of patients with coronary artery disease. Dobutamine stress echocardiography was used, a technique that allows direct visualisation of localised left ventricular dysfunction that occurs as a result of ischaemia. Dobutamine increases heart rate and contractility thus augmenting oxygen demand. In coronary artery disease, this increased demand leads to metabolic changes responsible for decreased wall thickness and abnormal wall motion.

Influence of treatment delay on long-term left ventricular function in patients with acute myocardial infarction successfully treated with primary angioplasty.

BACKGROUND: Myocardial salvage has been shown to be dependent on the time elapsed from the onset of acute myocardial infarction (AMI) to reperfusion. The aim of this study was to evaluate the importance of time to reperfusion for left ventricular function recovery after primary angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) for AMI. METHODS: Ninety-five patients undergoing long-term successful PTCA for AMI were studied. Echocardiography was performed before and 3, 7, 30, 90, and 180 days after PTCA. End-diastolic volume index (EDVI) and end-systolic volume index (ESVI), ejection fraction, and left ventricular wall motion score index (WMSI) were evaluated. RESULTS: Patients were divided into group A, 23 patients reperfused within 2 hours; group B, 32 patients reperfused between 2 and 4 hours; group C, 22 patients reperfused between 4 and 6 hours; and group D, 18 patients reperfused between 6 and 12 hours. Both EDVI and ESVI were reduced in groups A and B at 90 days. Groups C and D did not show any changes of EDVI and ESVI at any stage throughout the study. Ejection fraction improved only in groups A and B at 30, 90, and 180 days. At study entry, WMSI was similar in all groups. After 7 days, in group A and in group B, WMSI was improved, no changes were observed in group C, and a mild deterioration was observed in group D at 3 and 7 days. Subsequent evaluations showed progressive improvement of WMSI in all groups. CONCLUSIONS: Myocardial salvage is achieved only in patients revascularized within 4 hours from AMI onset. However, revascularization after 6 hours may be worthwhile by preventing ventricular remodeling.

Effect of sildenafil citrate upon myocardial ischemia in patients with chronic stable angina in therapy with beta-blockers.

BACKGROUND: It has been suggested that phosphodiesterase 5 (PDE5) inhibition is potentially hazardous and that it increases the risk of cardiac events in patients with coronary artery disease. This study sought to evaluate whether PDE5 inhibition with sildenafil exerts any effect on exercise-induced myocardial ischemia in patients on beta-blockers. METHODS: Fourteen patients underwent a baseline exercise test off-therapy and were then started on atenolol (100 mg once daily). After a run-in phase of 1 week, patients underwent a second exercise test and were randomized to receive either sildenafil (50 mg) or placebo given in a random order on two different occasions, 2 days apart. Exercise test was repeated 2 hours after the administration of sildenafil or placebo. RESULTS: All patients had a > 1 mm ST-segment depression while off-therapy. Eight patients had a negative exercise test response after atenolol, which was unaltered by the adjunct of either sildenafil or placebo. In the remaining subjects, atenolol significantly prolonged the time to 1 mm ST-segment depression and the exercise time. Sildenafil and placebo did not reverse the beneficial effect of atenolol upon exercise-induced myocardial ischemia. CONCLUSIONS: PDE5 inhibition does not worsen exercise capacity and exercise-induced myocardial ischemia in patients with chronic stable angina whose symptoms and exercise test response are well controlled by beta-blocker therapy.

Natural progesterone, but not medroxyprogesterone acetate, enhances the beneficial effect of estrogen on exercise-induced myocardial ischemia in postmenopausal women.

OBJECTIVES: We sought to compare the effects of estrogen/transvaginal progesterone gel with estrogen/medroxyprogesterone acetate (MPA) on exercise-induced myocardial ischemia in postmenopausal women with coronary artery disease or previous myocardial infarction, or both. BACKGROUND: Estrogen therapy beneficially affects exercise-induced myocardial ischemia in postmenopausal women; however, women with an intact uterus also take progestin to protect against uterine malignancies. The effects of combination estrogen/progestin therapy on myocardial ischemia are unknown. METHODS: Eighteen postmenopausal women (mean +/- SD age 59+/-7 years) were given 17-beta-estradiol in single-blinded manner for four weeks (1 mg/day for three weeks then 2 mg/day for one week). Estradiol (2 mg/day) was then continued, and the patients were randomized (double-blind) for 12 days to either transvaginal progesterone gel (90 mg on alternate days) and oral MPA placebo (10 mg/day), or vice versa. After another two weeks on estradiol alone, the patients crossed over to progestin treatment and repeated the protocol on the opposite treatment. Patients underwent treadmill exercise testing after each estradiol phase and at day 10 of each progestin phase. RESULTS: Exercise time to myocardial ischemia increased after the first estrogen phase as compared with baseline (mean difference with 95% confidence interval [CI]: 72 s [34 to 110], p = 0.001), and was increased by combination estradiol/progesterone therapy as compared with estradiol/MPA therapy (92 s [35 to 149], p = 0.001)). Two patients (11%) were withdrawn while taking estradiol/MPA owing to unstable angina. CONCLUSIONS: Combination estrogen/transvaginal progesterone gel increases exercise time to myocardial ischemia, as compared with estrogen/MPA. These results imply that the choice of progestin in women at higher cardiovascular risk requires careful consideration.

Acute electrophysiologic effect of estradiol 17beta in menopausal women.

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.

Circumferential radiofrequency ablation of pulmonary vein ostia: A new anatomic approach for curing atrial fibrillation.

BACKGROUND: The pulmonary veins (PVs) and surrounding ostial areas frequently house focal triggers or reentrant circuits critical to the genesis of atrial fibrillation (AF). We developed an anatomic approach aimed at isolating each PV from the left atrium (LA) by circumferential radiofrequency (RF) lesions around their ostia. METHODS AND RESULTS: We selected 26 patients with resistant AF, either paroxysmal (n=14) or permanent (n=12). A nonfluoroscopic mapping system was used to generate 3D electroanatomic LA maps and deliver RF energy. Two maps were acquired during coronary sinus and right atrial pacing to validate the lateral and septal PV lesions, respectively. Patients were followed up closely for >/=6 months. Procedures lasted 290+/-58 minutes, including 80+/-22 minutes for acquisition of all maps, and 118+/-16 RF pulses were deployed. Among 14 patients in AF at the beginning of the procedure, 64% had sinus rhythm restoration during ablation. PV isolation was demonstrated in 76% of 104 PVs treated by low peak-to-peak electrogram amplitude (0. 08+/-0.02 mV) inside the circular line and by disparity in activation times (58+/-11 ms) across the lesion. After 9+/-3 months, 22 patients (85%) were AF-free, including 62% not taking and 23% taking antiarrhythmic drugs, with no difference (P:=NS) between paroxysmal and permanent AF. No thromboembolic events or PV stenoses were observed by transesophageal echocardiography. CONCLUSIONS: Radiofrequency PV isolation with electroanatomic guidance is safe and effective in either paroxysmal or permanent AF.

Coronary angioplasty in patients with unstable angina: clinical, electrocardiographic and angiographic predictors of in-hospital outcome. R.OS.A.I. Study Group.

BACKGROUND: In unstable angina early coronary arteriography is frequently performed, often followed by percutaneous revascularization with liberal use of stents. We intended to study the in-hospital outcome of patients receiving this treatment. METHODS: From April 1997 to April 1998, patients submitted to coronary arteriography due to unstable angina, and with no previous myocardial revascularization, were included in a multicenter registry. RESULTS: Out of 987 patients enrolled at 14 centers, 876 (89%) had percutaneous or surgical revascularization. Coronary angioplasty was performed in 571 patients (58%); 281 (49%) had Braunwald class IIIB or C angina. Refractory or prolonged chest pain, or both, were present in 133, 217 and 85 patients, respectively, and multivessel disease in 245 patients (43%). Stenting was performed in 486/571 cases (85%), abciximab was administered to 42 patients, and ticlopidine and/or aspirin to all. A procedural success was obtained in 96.9 % of cases. In-hospital major adverse cardiac events occurred in 29/571 patients (5.1%). Pain-related ST segment depression (44% of cases) was not predictive of outcome after coronary angioplasty. In multivariate analysis prolonged plus refractory angina (p = 0.02), an ejection fraction < 0.4 (p = 0.04), multivessel disease (p = 0.01) and--with the strongest predictive value--ad hoc angioplasty (p = 0.007) and use of > 1 stent (p = 0.0008) were all independent predictors of in-hospital adverse outcome. CONCLUSIONS: Coronary angioplasty with a liberal use of stents yields a high rate of procedural success, with few in-hospital major cardiac events also in "high risk" patients.

Detrimental effects of acute heparin administration on ischemic threshold in patients with coronary artery disease.

BACKGROUND: Recent studies have indicated that heparin administration might decrease endothelial nitric oxide production. The aim of this study was to investigate the effect of heparin on ischemic threshold. METHODS: Eighteen patients with a positive exercise test and proven coronary artery disease were submitted to a randomized, placebo-controlled trial using i.v. 0.9% NaCl as placebo and i.v. heparin (5,000 IU bolus + 1,000 IU/h). After both saline and heparin bolus, the infusion was started and, after 10 min, the exercise test was performed. Blood samples for nitric oxide metabolites and free fatty acid determinations were taken before, at peak exercise, and at ECG recovery. RESULTS: As compared to placebo, heparin significantly decreased time to 1 mm ST segment depression (241 +/- 160 vs 303 +/- 175 s, p = 0.003) and prolonged recovery (573 +/- 177 vs 441 +/- 195 s, p = 0.003), while exercise duration was similar. Accordingly, rate-pressure product at 1 mm ST segment depression was lower after heparin, while it was similar at peak exercise. No significant differences were found for plasma nitric oxide metabolite levels. Conversely, free fatty acid levels were higher after heparin throughout the study in all patients. The increase in free fatty acids was not correlated with the difference in rate-pressure product at 1 mm ST segment depression between placebo and heparin (r = 0.34, p = NS). CONCLUSIONS: In patients with stable coronary artery disease, heparin significantly decreased exercise ischemic threshold. The lower rate-pressure product at 1 mm ST segment depression during heparin, compared to placebo, suggests an impairment of coronary blood flow, which does not seem to be mediated by decreased nitric oxide production/release. The increased free fatty acid release, on the other hand, might contribute to the detrimental effect of heparin on exercise-induced ischemia, but the lack of a correlation with changes in ischemic threshold suggests that other, still unknown, factors are involved.

Heart rate variability in patients with variant angina: effect of the presence of significant coronary stenosis.

BACKGROUND: The syndrome of variant angina occurs in patients with a wide spectrum of coronary disease ranging from angiographically normal coronary arteries to severe three-vessel disease. Survival and choice of therapy for these patients are determined by the extent of underlying fixed coronary obstruction. We examined whether heart rate variability (HRV) due to reduced vagal outflow may correlate with the severity of coronary stenoses in such patients. METHODS: Fifteen men and 2 women with clinically unstable variant angina underwent 24-hour Holter monitoring from which low and high-frequency power, standard deviation of mean 24-hour RR interval, proportion of adjacent RR intervals that differed by more than 50 ms, and mean root square of differences between successive RR intervals were extracted by power spectral analysis. Coronary angiography was later performed to determine coronary pathology and verify variant angina. As controls we studied an age-matched control group of 8 subjects (5 men, 3 women) with no clinical and/or electrocardiographic evidence of coronary heart disease or spasm as shown by negative treadmill exercise and hyperventilation tests. RESULTS: All measured components of HRV were significantly lower in the 9 patients with severe coronary artery disease compared to the 8 patients with normal coronary arteries or < 40% stenosis. The two groups were otherwise similar in terms of age and clinical parameters. CONCLUSIONS: These preliminary findings on a small but carefully selected group of patients with variant angina indicate that the analysis of HRV can select patients with severe disease for a more intensive approach. These findings require confirmation on a larger patient series.

[The primary and secondary prevention of ischemic cardiopathy]. / Prevenzione primaria e secondaria della cardiopatia ischemica.

The aim of this paper was to summarize the most important clinical issues on coronary artery disease prevention, in order to provide the best advice to cardiologists, and facilitate their work on primary and secondary prevention. Although in recent years the knowledge of the beneficial effects of major risk factor modification has been increasing, most physicians still concentrate only on patients with overt coronary artery disease. Many high-risk individuals are not adequately advised and treated, whilst a great effort should be made by national institutions and individual doctors to implement primary prevention schemes. Indeed, the potential for preventive measures is greatest in high-risk groups. Specific international task forces have issued official recommendations on the prevention of coronary heart disease in clinical practice, which have been intended to encourage the development and revision of national guidelines on coronary prevention. The challenge for cardiologists in the year 2000 is to realize the potential for coronary prevention in all patients, and to contribute to reduce the enormous socio-economic burden of cardiovascular disease.

The role of myocardial viability in deriving benefit from reestablishing infarct-related artery flow after acute myocardial infarction.

Early, sustained patency of the infarct-related artery (IRA) induces myocardial salvage, which preserves left ventricular (LV) function and mediates better long-term outcome. However, the time course and the mechanisms of muscle recovery after myocardial infarction are not completely understood. A large body of evidence suggests that most of the improvement occurs during the hospital phase and is related to early and sustained thrombolysis in myocardial infarction 3 flow in the IRA. Nevertheless, the relationship between IRA status and regional and global LV mechanics in the chronic phase of the disease remains controversial. Some late recovery may occur, either spontaneously or after revascularization, even in the absence of documented myocardial ischemia. The interplay between vessel patency, coronary flow grade and severity of the residual stenosis, and the presence of stunned or hibernating myocardium in the area at jeopardy may explain this delayed improvement. Although there seems to be a limited time window in which myocardium can be salvaged, timely testing for viability, particularly in patients with poor LV function, is justified even in a later phase of the disease to challenge potential cardiac recovery.

Enoximone echocardiography for predicting recovery of left ventricular dysfunction after revascularization : a novel test for detecting myocardial viability.

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 microg. 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<0.01) and negative predictive value (90% versus 84%, P<0.05) in predicting functional recovery. The specificity (89% versus 90%) and positive predictive value (87% for both EE and DE) were similar. Concordant interpretation of EE and DE findings was found in 85% (406 of 478) of affected segments. Prerevascularization coronary angiography showed that stenosis severity of vessels supplying areas which only improved with enoximone was significantly greater (89.9%) than that of vessels (77.7%) supplying areas that responded to both agents (P<0.02). Both dobutamine and enoximone increased heart rate (16% and 10%, respectively), whereas enoximone did not cause changes in systolic blood pressure that increased by 14% with dobutamine. 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.