Do We Need Fasting Prior to Coronary Angiography? The CORO-NF Randomized Pragmatic Study.

BACKGROUND: Similar to procedures requiring general anesthesia, current guidelines recommend fasting for 6 hours for solids and for 2 hours for liquids prior to coronary angiography, but without data supporting such recommendation. The CORO-NF study aimed at assessing whether a shorter fasting period prior to elective coronary angiography associates with improved patient satisfaction without more complications compared with the standard fasting approach. METHODS: We conducted a single-center, randomized, prospective, pragmatic study in 2 sequential phases: a "conventional protocol phase," continuing the usual practice (F Group); and an "experimental phase" (NF Group), reducing minimum fasting duration to 2 hours. Patients received a questionnaire to express a satisfaction score ranging from 1 (maximum complain/no approval) to 5 (minimum or no complain/full approval). All patients admitted acutely were enrolled in a control A Group registry. Fasting time and every major complication and periprocedural complications were analyzed. RESULTS: Fasting time was 821 ± 357 minutes in the F Group and 230 ± 146 minutes in the NF Group (P < .001). The satisfaction score was higher in the NF Group (4.2 ± 0.7 vs 2.9 ± 1.2, P < .001), even at multivariable analysis considering fasting time (P < .001). No intraprocedural food ingestion-related adverse events occurred in either of the 2 experimental groups, as well as in the parallel A Group, with no excess of peri- and postprocedural complications in the NF Group. CONCLUSIONS: The significantly higher satisfaction scores among patients undergoing a shorter-than-recommended fasting period prior to coronary angiography, not counterbalanced by decreased safety, underscores the potential benefits of revising the traditional 6-hour fasting protocols.

Glucose tolerance and markers of myocardial injury after an acute coronary syndrome: predictive role of the 1-h plus 2-h plasma glucose at the oral glucose tolerance test.

OBJECTIVE: Impaired glucose tolerance (IGT) has been related to adverse cardiovascular outcomes. We investigated the added value of 1-h plasma glucose (PG) at the oral glucose tolerance test (OGTT) in predicting admission and peak cardiac high-sensitivity troponin T (hs-TnT) and NT-proBNP values in IGT patients admitted for an acute coronary syndrome (ACS). RESEARCH DESIGN AND METHODS: Among 192 consecutive ACS patients, 109 had Hb1Ac and fasting plasma glucose negative for newly diagnosed diabetes. Upon OGTT performed > 96 h after admission, 88, conventionally diagnosed as IGT, were divided into: "full glucose tolerance" (1-h PG-OGTT < 155 mg/dL and 2-h PG-OGTT < 140 mg/dL, N = 12);"early IGT" (1 h-PG-OGTT ≥ 155 mg/dL and 2-h PG-OGTT < 140 mg/dL, N = 33);"late IGT" (1-h PG-OGTT < 155 mg/dL and 2-h PG-OGTT ≥ 140 mg/dL, N = 8); and "full IGT" (1-h PG-OGTT ≥ 155 mg/dL and 2-h PG-OGTT ≥ 140 mg/dL, N = 35). The 4 groups were compared for cardiac markers. RESULTS: The first three groups had similar cardiac marker values, but only full IGT patients had significantly higher admission hs-TnT compared with the 3 other groups [median (interquartile range): 911 (245-2976) vs 292 (46-1131), P < 0.001]. Full IGT patients also had higher hs-TnT peak compared with fully glucose tolerant and early IGT patients. Only full IGT patients had longer hospitalization and higher NT-proBNP vs fully glucose tolerant patients (P = 0.005). CONCLUSIONS: Among non-diabetic ACS patients, only those with both 1-h PG ≥ 155 mg/dL and 2-h PG ≥ 140 mg/dL had more severe myocardial injury and longer hospitalization. One-h PG-OGTT importantly contributes to assessing post-ACS cardiac risk.

The non-vitamin K antagonist oral anticoagulants and heparin-induced prolongation of the activated coagulation time.

BACKGROUND AND AIMS: Unfractionated-heparin (UFH) is the first-choice parenteral anticoagulant during invasive percutaneous procedures and its effect is monitored by the activated coagulation time (ACT). The effects of the non-vitamin K antagonist oral anticoagulants (NOACs) on the ACT and on ACT prolongation by UFH were not clearly established. We assessed the ACT prolongation induced by different UFH concentrations in blood samples of patients taking the four types of currently marketed NOACs and in patients not taking anticoagulants. METHODS AND RESULTS: We measured the ACT in patients on dabigatran 110 mg (n = 8), rivaroxaban (n = 10), apixaban (n = 9) and edoxaban (n = 10) at supposed peak plasma concentrations, before and after in vitro addition of 3 UFH concentrations, corresponding to doses of 2000, 5000 and 10,000 IU. Seven non-anticoagulated patients served as controls. Patients in the 5 groups did not differ significantly for age, body weight and glomerular filtration rate. Baseline ACTs (s, mean ± SD) were 192 ± 27, 124 ± 14, 132 ± 14, 151 ± 30 and 134 ± 7 in dabigatran 110, rivaroxaban, apixaban, edoxaban and controls, respectively (P < 0.05 for dabigatran vs the other NOACs). We found a linear prolongation of the ACT with the in vitro UFH addition (P < 0.001), but prolongation was similar between the NOACs and controls. CONCLUSIONS: Dabigatran induces a moderate, significant ACT prolongation. None of the NOACs affects the UFH-induced ACT prolongation in the commonly used UFH range. The dose of UFH currently recommended to achieve the target ACT should thus be used irrespective of whether patients are taking NOACs or not.

A case report of multisite arterial thrombosis in a patient with coronavirus disease 2019 (COVID-19).

BACKGROUND: A systemic coagulation dysfunction has been associated with COVID-19. In this case report, we describe a COVID-19-positive patient with multisite arterial thrombosis, presenting with acute limb ischaemia and concomitant ST-elevation myocardial infarction and oligo-symptomatic lung disease. CASE SUMMARY: An 83-year-old lady with history of hypertension and chronic kidney disease presented to the Emergency Department with acute-onset left leg pain, pulselessness, and partial loss of motor function. Acute limb ischaemia was diagnosed. At the same time, a routine ECG showed ST-segment elevation, diagnostic for inferior myocardial infarction. On admission, a nasopharyngeal swab was performed to assess the presence of SARS-CoV-2, as per hospital protocol during the current COVID-19 pandemic. A total-body CT angiography was performed to investigate the cause of acute limb ischaemia and to rule out aortic dissection; the examination showed a total occlusion of the left common iliac artery and a non-obstructive thrombosis of a subsegmental pulmonary artery branch in the right basal lobe. Lung CT scan confirmed a typical pattern of interstitial COVID-19 pneumonia. Coronary angiography showed a thrombotic occlusion of the proximal segment of the right coronary artery. Percutaneous coronary intervention was performed, with manual thrombectomy, followed by deployment of two stents. The patient was subsequently transferred to the operating room, where a Fogarty thrombectomy was performed. The patient was then admitted to the COVID area of our hospital. Seven hours later, the swab returned positive for COVID-19. DISCUSSION: COVID-19 can have an atypical presentation with thrombosis at multiple sites.

High sensitivity cardiac troponins: Can they help in diagnosing myocardial ischaemia?

BACKGROUND: Cardiac troponin is the most sensitive marker of myocardial injury, but controversy still exists about its role in detecting ischaemia. METHODS: To investigate the role of troponin as a marker of stress-induced ischaemia, circulating high sensitivity cardiac troponin T (hs-cTnT) was measured and compared with the MB fraction of creatine kinase (CK-MB) in 125 patients undergoing a stress test (53 electrocardiogram/echo exercise, 42 echo dipyridamole and 30 echo dobutamine tests). RESULTS: Plasma concentrations of hs-cTnT increased after the tests in 90/125 patients, while an increase of CK-MB was seen in 31/125 patients ( p<0.0001). Overall, hs-cTnT significantly increased from 17.5±16.9 ng/l to 25.5±27.9 ng/l ( p<0.0001), without significant changes of CK-MB. Significant increments in hs-cTnT were documented after exercise test (from 15.9±11.9 ng/l to 19.5±13.6 ng/l, p<0.0001) and dobutamine test (from 20.6±20.8 ng/l to 37.8±31.1 ng/l, p=0.0006), in absence of changes in CK-MB according to each stressor. Among the 125 tests, 84 were diagnosed as negative and 41 as positive for myocardial ischaemia. Significant increments in hs-cTnT were detected after both negative (from 18.6±19.2 ng/l to 27.1±32.1 ng/l, p=0.0018) and positive test (from 15.2±10.8 ng/l to 22.3±16.2 ng/l, p=0.0005), without significant changes of CK-MB according to the test result. Despite a positive correlation between stress-induced increase of hs-cTnT and obstructive coronary artery disease, the release of troponin was observed also in a significant proportion of patients without coronary stenoses. Left ventricular hypertrophy markedly enhanced myocardial release of troponin. CONCLUSIONS: Circulating troponin increases in most patients undergoing a stress test, irrespective of the test result and of coronary artery disease. Plasma release of troponin depends on multiple pathogenetic mechanisms, making the biomarker a not reliable tool in detecting transient ischaemia.

Interactions Between Reciprocal ST-Segment Downsloping During ST-Elevated Myocardial Infarction and Global Cardiac Perfusion and Functional Abnormalities.

Reciprocal ST-segment downsloping on electrocardiogram is a frequent finding during ST-elevated myocardial infarction (STEMI), but its etiology is still disputed. We sought to evaluate the relation between reciprocal ST-segment downsloping during STEMI and major cardiac perfusion and functional parameters. One hundred eighty-five patients with STEMI underwent emergency coronary angiography. The presence of reciprocal ST-segment downsloping was assessed. At coronary angiography, the corrected TIMI frame count (cTFC) was computed both on culprit and remote vessels and the occurrence of "no/slow reflow" phenomenon after percutaneous coronary intervention (PCI) identified. The left ventricular wall motion score index ratio (discharge/admission values) at echocardiography and the slope of high-sensitivity troponin elimination were computed as measures of effective myocardial reperfusion. Reciprocal ST-segment downsloping was revealed in 91 patients (49%). They presented higher cTFC values on remote vessels than patients without reciprocal electrocardiographic abnormalities (44 ± 18 vs 37 ± 15 cineframes × second-1, p = 0.004). The presence of remote ST-segment downsloping was also associated with a higher prevalence of "no/slow reflow" phenomenon (59% vs 40%, p = 0.013) as well as more abnormal values of wall motion score index ratio (p = 0.042) and high-sensitivity troponin slope (p = 0.012). At multivariate analyses, a higher cTFC on remote vessels predicted the occurrence of reciprocal ST-segment changes (p = 0.018) and the development of "no/slow reflow" phenomenon after PCI (p = 0.005). In conclusion, the presence of reciprocal ST-segment downsloping during STEMI clusters with significant perfusion and cardiac functional abnormalities, predicting the development of "no reflow" phenomenon after PCI.

Association of furosemide dose with clinical status, left ventricular dysfunction, natriuretic peptides, and outcome in clinically stable patients with chronic systolic heart failure.

In chronic heart failure (HF), high daily doses of furosemide have been associated with increased mortality. The authors sought to evaluate the relationships between orally administered furosemide doses, clinical status, left ventricular (LV) dysfunction, N-terminal proBNP (NT-proBNP), and outcome in 400 outpatients with chronic HF and LV ejection fraction (EF) ≤ 45%. Clinical status, NT-proBNP levels, and estimated glomerular filtration rate (eGFR) were evaluated. Median follow-up duration was 32 months. The median values of daily-dose furosemide and of furosemide dose normalized to body surface area were 25 mg (12.5-62.5 mg) and 15 mg/m(2) (13-34 mg/m(2)), respectively. A total of 32% of patients had decompensated HF according to Framingham score and criteria for congestion. In clinically stable patients, a multivariable Cox model, which included clinical and echocardiographic parameters plus NT-proBNP, hemoglobin, and eGFR, showed that normalized furosemide dose (P=.017), anemia (P=.060), age (P=.080), and New York Heart Association class (P=.080) were predictors of all cause-mortality. In patients with decompensated HF, LV end-systolic volume index (P=.018), NT-proBNP (P=.060), and reduced eGFR (P=.070) were independently related to the outcome. Normalized furosemide dose was a major determinant of prognosis in patients with chronic HF but without ongoing signs and symptoms, and this suggests a possible negative interaction of this drug in clinically stable patients.

Right ventricular dysfunction is associated with chronic kidney disease and predicts survival in patients with chronic systolic heart failure.

AIMS: Chronic kidney disease (CKD) and right ventricular (RV) dysfunction are important predictors of prognosis in heart failure (HF). We investigated the relationship between RV dysfunction and CKD in outpatients with chronic systolic HF, an association which remains poorly defined. METHODS AND RESULTS: Outpatients (n = 373) with chronic HF and left ventricular ejection fraction (LVEF) ≤45% underwent clinical and echo-Doppler evaluations and were followed up for 31 ± 24 months. Tricuspid annular plane systolic excursion (TAPSE) assessed RV dysfunction. The estimated glomerular filtration rate (GFR) was measured by the simplified Modification of Diet in Renal Disease (MDRD) formula. Correlation analysis was used to characterize the association between TAPSE and estimated GFR. Odds ratios (ORs) for CKD and hazard ratios (HRs) for all-cause mortality were assessed using multivariable logistic or proportional hazards regression models. TAPSE and estimated GFR were significantly correlated (r = 0.38, P < 0.0001). TAPSE ≤14 mm was associated with elevated estimated right atrial pressure and N-terminal pro brain natriuretic peptide levels. TAPSE ≤14 mm increased the odds of estimated GFR <60 mL/min/1.73 m(2), OR [95% confidence interval (CI)] = 2.51(1.44-4.39), P < 0.0001 and predicted all-cause mortality, HR (95% CI) = 1.80 (1.20-2.71) after multivariable adjustment. CONCLUSIONS: Right ventricular dysfunction is cross-sectionally associated with CKD and prospectively predicts survival in outpatients with chronic systolic HF. These data suggest RV dysfunction to be one of the possible mechanistic links between HF and CKD.

Admission C-reactive protein serum levels and survival in patients with acute myocardial infarction with persistent ST elevation.

OBJECTIVE: To evaluate the prognostic value of a single and early determination of high sensitivity C-reactive protein levels at admittance in patients with acute myocardial infarction with persistent ST elevation. PATIENTS AND METHODS: We evaluated high-sensitivity C-reactive protein levels in 247 consecutive acute myocardial infarction with persistent ST elevation patients at admittance. Patients were monitored for the occurrence of major adverse cardiovascular events. RESULTS: Mean follow-up was 26 months. High C-reactive protein levels were principally associated with age > or = 65 years (P=0.01), diabetes (P=0.03) and reduced left ventricle ejection fraction (P=0.048). We observed a significant C-reactive protein level difference between the major adverse cardiovascular event-free group and the major adverse cardiovascular event group (28.2+/-21.9 vs. 47.7+/-31.9 mg/l, P=0.03), between deceased patients group (vs. 81.5+/-51.8 mg/l, P<0.001) and early deaths (vs. 129.5+/-71.9 mg/l, P<0.001). Kaplan-Meier plots for survival and major adverse cardiovascular event occurrence showed a significant separation (P=0.01 and 0.002 by log-rank test, respectively) between high and low C-reactive protein level groups. C-reactive protein levels were independent risk predictors of major adverse cardiovascular events (odds ratio 2.931, 95% confidence interval 1.512-5.893; P=0.046) and death (odds ratio 5.068, 95% confidence interval 2.056-20.195; P=0.04). Patients with high C-reactive protein levels and age > or = 65 years were at highest risk for major adverse cardiovascular event occurrence (odds ratio 5.658, 95% confidence interval 2.898-6.249; P=0.022) and death (odds ratio 8.120, 95% confidence interval 5.656-22.729; P=0.03). CONCLUSIONS: High C-reactive protein levels identify patients with a worse prognosis after acute myocardial infarction with persistent ST elevation. The evaluation of C-reactive protein and age may provide a tool to select high-risk patients.

A case of acute myocardial infarction during 5-fluorouracil infusion.

Cardiac toxicity is an uncommon side-effect of 5-fluorouracil (5-FU) treatment, consisting mainly of chest pain episodes with or without electrocardiographic changes and dysrhythmias. Here, we describe the case of a 56-year-old male patient with a diagnosis of advanced colorectal cancer who developed an acute myocardial infarction during 5-FU infusion. The patient was not affected by prior heart disease and did not show any classic risk factors for coronary heart disease. Coronary angiography examination revealed no evidence of coronary stenosis, supporting the hypothesis of a coronary artery spasm related to 5-FU infusion. Given the great number of cancer patients receiving 5-FU containing chemotherapeutic regimens, this rare but severe cardiac side-effect may be observed in both cardiologic and oncologic clinical practice. We suggest a tight clinical monitoring of all patients receiving 5-FU infusions, even in those without a prior history of heart disease.

Myocardial function in severe aortic stenosis before and after aortic valve replacement: a Doppler tissue imaging study.

BACKGROUND: The aim of the study was to assess the value of Pulsed-wave Doppler tissue imaging (DTI) in assessing diastolic and systolic function in patients with severe aortic value stenosis. METHODS: Thirty-five patients with aortic stenosis (AS) (valve orifice < or = 1 cm 2 , mean age 71.8 +/- 6.2) and 35 comparable healthy subjects were studied. All subjects performed conventional 2-dimensional Doppler echocardiography and DTI at mitral annulus level. Patients with AS were divided into 2 groups: 16 patients who presented initial signs of HF and a depressed left ventricular systolic function (AS I) (EF: 35%-50%) and 19 patients were asymptomatic and had normal left ventricular systolic function (EF > 50%) (ASII). The 16 symptomatic AS patients underwent surgical aortic valve replacement and were examined after 1 year. RESULTS: DTI was able to detect abnormalities of systolic and diastolic function in AS: the significantly lower peak S velocity in AS I than in AS II and in controls, both at septum and lateral wall level; the significantly lower peak E velocity in AS I than in AS II and in controls both at septum and lateral wall level; the significantly higher peak A velocity in AS I than in AS II and in controls both at septum and lateral wall level; the significant lower E/A ratio in AS I than in AS II and in controls both at septum and lateral wall level. CONCLUSION: We found a significant inverse correlation between DTI lateral S velocity, DTI peak E velocity, lateral DTI E/A ratio, and AS peak and mean gradient. According to the results of this study we can affirm that DTI parameters surely had an important physiopathological impact in the knowledge of myocardial function in patients with severe aortic stenosis.

Left ventricular hypertrophy and its regression in essential arterial hypertension. A tissue Doppler imaging study.

The mitral annulus velocities of Doppler transmitral flow and pulsed-wave tissue Doppler imaging (TDI) were sampled by echocardiography for the assessment of left ventricular (LV) diastolic function in 118 never-treated essential hypertensive patients with normal systolic function and compared with those of 59 normotensive healthy subjects matched for age and sex. A selected group (n = 26) of the hypertensive study population was observed after 1 year of pharmacologic antihypertensive treatment to determine the behavior of TDI parameters in relation to eventual regression of LV hypertrophy (LVH). We found that the TDI early myocardial diastolic wave (E(m)) was significantly lower both in concentric and eccentric LVH. In addition, TDI late myocardial diastolic wave (A(m)) was significantly higher in concentric remodeling and concentric and eccentric hypertrophy. The TDI E(m)/A(m) ratio was significantly lower in all geometric remodeling subgroups. The E/A ratio Doppler transmitral flow velocity measured showed that of the 118 patients, only 32 (25%) could really be discriminated from normal, whereas individual analysis for TDI E(m)/A(m) at the mitral annulus septal level showed that of 118 patients 108 (91%) could be discriminated from normal P < .001). The LV mass was significantly less after 1 year of treatment (LVH regression), and TDI parameters showed a trend toward normalization, in particular of TDI E(m)/A(m) at the annular septal level. Pulsed-wave TDI analysis could enable not only the early assessment of whether a patient is still in an adaptive or compensatory phase before transition to irreversible damage (pathologic phase) but also the detection of precocious LV global diastolic dysfunction. With regard to this, more extensive randomized studies are needed to evaluate the effect of different pharmacologic treatments (calcium antagonists, beta-blockers, angiotensin I and II inhibitors) on TDI parameters.

"Torsade de pointes" in a patient with variant angina.

Ventricular tachyarrhythmias have been well documented in patients with variant angina. Episodes of torsade de pointes have been described infrequently. We report a case of a 60-year-old male with a previous history of one vessel artery disease and a successful coronary angioplasty with stenting of the left anterior descending artery, who experienced an episode of angina at rest and electrocardiographic evidence of self-terminating torsade de pointes. After a negative coronary angiography and a positive hyperventilation test, the diagnosis of variant angina was considered and beta-blockers discontinued and calcium channel antagonists prescribed. No other episodes of angina were documented during the following 6 months of follow-up.

Role of platelet glycoprotein IIb/IIIa inhibitors in rescue percutaneous coronary interventions.

In the setting of acute myocardial infarction, thrombolytic therapy fails to restore an adequate epicardial flow in a large number of patients. Although an increasing number of patients undergoes a percutaneous coronary intervention (PCI) after failed thrombolysis, this treatment has been poorly investigated. This review focuses particularly on the safety and prognostic impact of glycoprotein (GP) IIb/IIIa receptor inhibitors after failed thrombolysis. GPIIb/IIIa inhibitors have been demonstrated to improve the clinical outcome in patients undergoing primary PCI. However, the increased risk of bleeding with the administration of potent antiplatelet drugs after full-dose thrombolytics has limited the widespread use of GPIIb/IIIa inhibitors during rescue PCI. We recently reported that abciximab treatment during rescue PCI has a beneficial effect on the short-term prognosis, without excess bleeding complications. This result can be achieved by using the radial approach, a low-dose weight-adjusted heparin regimen, and by limiting the use of aortic counterpulsation. In conclusion, in case of thrombolysis failure, patients should be referred to tertiary hospitals where rescue PCI can be performed with expertise.

[Type-A aortic dissection without chest pain in a patient with Clostridium fallax infection]. / Dissezione aortica tipo A in un paziente con setticemia da Clostridium fallax asintomatico per dolore toracico.

We describe the case of a 64-year-old patient admitted to our hospital because of syncope and suspicion of cardiac tamponade. At admission he had temporary alteration of conscience with clinical evidence of sepsis without chest pain. There was a mild pericardial effusion in absence of clinical and echocardiographic signs of cardiac tamponade. About 36 hours later we found evidence of an aortic dissection and in the blood culture an isolation of Clostridium fallax that we consider the probable cause of this lesion.

Usefulness of intravenous myocardial contrast echoardiography in the early left ventricular remodeling in acute myocardial infarction.

The aim of this study was to assess the role of intravenous myocardial contrast echocardiography (IMCE) in the prediction of left ventricular (LV) remodeling in patients with acute myocardial infarction (AMI). Sixty-three patients with AMI, who were successfully treated with acute coronary angioplasty, underwent IMCE and low-dose dobutamine echocardiography during hospital admission. IMCE was graded semiquantitatively on a score of 0 (no visible contrast effect), 0.5 (patchy myocardial contrast enhancement), and 1 (homogenous contrast effect). Patients were considered to have microvascular impairment if <50% of segments within the infarct-related area had score of 1. A mean perfusion score index was calculated for each patient. Patients with a good perfusion at IMCE (IMCE+) showed a lower creatine kinase peak (p = 0.001) and lower creatine kinase-MB (p = 0.01), and a better baseline regional contractile function compared with patients who had negative results at IMCE (IMCE-) (p <0.0001) and a higher amount of myocardial viability at low-dose dobutamine echocardiography (p = 0.03). At follow-up, a higher improvement in regional systolic function (p = 0.0006) was observed in IMCE+ patients, whereas IMCE- patients showed an evident increase in LV end-diastolic volume from baseline to 6-month follow-up (p <0.0001), implying LV remodeling, which has been associated with a higher incidence of adverse cardiac events (p = 0.005). By stepwise multiple regression analysis, microvascular impairment at IMCE was a significant independent predictor of LV remodeling (p <0.0001). Thus, IMCE seems to be an important diagnostic tool, able to predict LV remodeling in patients with AMI.

P-wave signal-averaged electrocardiogram predicts atrial fibrillation after coronary artery bypass grafting.

BACKGROUND: AF is one of the most common complications after CABG. The aim of the study was to identify the risk factors for postoperative AF. METHODS: Between June and December 2000, 129 consecutive patients (72 men, 47 women; mean age 67 +/- 6 years) underwent preoperative signal-averaged electrocardiogram (SAECG) with assessment of filtered P-wave duration (fPWD) and of the root mean square voltage of the last 10 and 20 ms of atrial depolarization (RMSV10 and RMSV20, respectively) before CABG. RESULTS: Fifty-six (43%) patients developed one episode of AF lasting > 30 seconds at a mean distance of 2.6 +/- 1.8 days after surgery (group A), while 73 patients remained in sinus rhythm (group B). No differences between the two groups were found in terms of age, sex, P-wave duration on the standard ECG, left atrial dimensions, and operative characteristics. In contrast, group A patients showed a significantly longer fPWD (138 +/- 10 vs 111 +/- 9 ms; P < 0.001) and smaller RMSV10 and RMSV20 (2.8 +/- 1.0 vs 4.3 +/- 1.1 microV, P < 0.001; 4.2 +/- 2.1 vs 6.2 +/- 2.0 microV, P < 0.001). Multivariate analysis indicated only fPWD as an independent predictor of AF (P = 0.009). With a cut-off value of 135 ms for fPWD, the occurrence of AF could be predicted with a sensitivity of 84%, a specificity of 73%, a negative predictive value of 85%, and a positive predictive value of 70%. CONCLUSION: Preoperative SAECG is a simple exam that correctly identifies patients at higher risk of AF after CABG. A more widespread use of this technique can be suggested.

Abciximab improves 6-month clinical outcome after rescue coronary angioplasty.

BACKGROUND: Few data are available concerning the effects on clinical outcome and left ventricular function of abciximab administration in patients undergoing rescue percutaneous transluminal coronary angioplasty (PTCA) after failed thrombolysis for acute myocardial infarction. The aim of the study was to investigate such effects. METHODS: Eighty-nine consecutive patients referred to our laboratory from other hospitals for rescue PTCA within 24 hours from the onset of chest pain were prospectively randomized before the procedure to abciximab treatment (44 patients) or placebo (45 patients). No significant differences in baseline characteristics were observed between the 2 groups. Study end points were the occurrence of major adverse cardiac events (MACE) such as death, reinfarction, congestive heart failure, target lesion revascularization, or recurrent ischemia at 30-day and 6-month follow-up and the occurrence of periprocedural bleeding. RESULTS: Mean time from symptom onset to reperfusion was 8.5 +/-5.4 hours; rescue PTCA was successful in 96% of patients. The incidence of major, moderate, and minor bleeding was similar in the 2 groups. At 30-day follow-up, the echocardiographic left ventricular wall motion score index showed a significantly higher improvement in the abciximab group versus the placebo group (P <.001). At 6-month follow-up, the incidence of MACE was 11% in the abciximab group versus 38% in the placebo group (P =.004). Abciximab administration (P =.003) and cardiogenic shock (P =.005) were the only independent predictors of the occurrence of MACE at multivariable analysis. CONCLUSION: Treatment with abciximab during rescue PTCA positively affects clinical outcome at 6-month follow-up without increasing periprocedural bleeding.