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Background —In patients with acute myocardial infarction (AMI) undergoing thrombolytic therapy, an elevated troponin level on admission is associated with a lower reperfusion rate and a complicated clinical course. Whether an elevated troponin level on admission similarly predicts an adverse outcome in patients undergoing primary angioplasty is currently unknown and was investigated in the present study. Methods and Results —Cardiac troponin I (cTnI) was determined on admission in 110 consecutive patients with AMI associated with ST-segment elevation or left bundle branch block who underwent primary angioplasty. Fifty-four patients (49%) had an elevated cTnI (≥0.4 ng/mL) on admission. In patients with elevated cTnI, primary angioplasty was less likely to achieve TIMI 3 flow (as classified by the Thrombolysis in Myocardial Infarction trial) in univariate (76% versus 96%, P =0.03) or in multivariate (odds ratio 0.1, 95% CI 0.02 to 0.54) analysis. Patients with elevated cTnI were more likely to develop congestive heart failure (23% versus 9%, P P =0.006). Elevated cTnI remained a significant predictor of the composite end point after controlling for other clinical data that were available early in the course, including time to presentation and angiographic results (relative risk 5.2, 95% CI 1.03 to 26.3). During a follow-up of 426±50 days, elevated admission cTnI was a predictor of cardiac mortality (11% versus 0%, P =0.012), adverse cardiac events (cardiac mortality or nonfatal reinfarction; 19% versus 5.4%, P =0.04), and adverse cardiac events plus target vessel revascularization (32% versus 14%, P =0.054). Conclusions —In patients with ST-segment elevation AMI, an elevated cTnI on admission is associated with an increased risk of primary angioplasty failure and a more complicated clinical course.

We investigated survival of patients with out-of-hospital cardiac arrest in Ljubljana according to the 'Utstein' style. Ljubljana consists of urban, suburban and semi-rural communities which encompass an area of 1615 km2 with 397306 residents. The area is served by a single response emergency medical system and local family practitioners. Between January 1, 1995 and December 31, 1997 cardiac arrest was confirmed in 966 patients. Cardiopulmonary resuscitation was attempted in 454 patients (47%). Collapse of presumed cardiac etiology (337 patients) was either bystander-witnessed (89%), un-witnessed (9%) or EMS personnel-witnessed (2%). Asystole was documented in 55%, ventricular fibrillation or tachycardia in 36% and other non-perfusing rhythms in 9% of these patients. Lay-bystander basic life support was performed in 19%. Nineteen patients (5.6%) survived to hospital discharge and 12 of them were independent in daily life. The survival of subgroups with bystanders-witnessed collapse and bystanders-witnessed ventricular fibrillation was 6.4 and 13%, respectively. Collapse of non-cardiac etiology (117 patients) was preceded by either respiratory failure (41), politrauma (22), circulatory shock (19), cerebrovascular incident (ten), intoxication (nine), strangulation (seven), electrocution (five) or drowning (four patients). Only five patients (4.2%) survived to hospital discharge. Hospital treatment of patients after successful initial cardiopulmonary resuscitation was associated with high mortality and required considerable resources.

Study objectives To evaluate the diagnostic value of transesophageal echocardiography (TEE) as an initial diagnostic tool in shocked patients. The second objective was to study therapeutic impact of intrapulmonary thrombolysis in patients with diagnosed massive pulmonary embolism. Design Prospective observational study. Setting Medical ICU in 800-bed general hospital. Patients Twenty-four consecutive patients with unexplained shock and distended jugular veins. Measurements and main results In 18 patients, right ventricular dilatation with global or segmental hypokinesis was documented. In addition, central pulmonary thromboemboli (12 patients), reduced contrast flow in right pulmonary artery (one patient), and right ventricular free wall akinesis (one patient) were found. No additional echocardiographic findings were apparent in four patients. According to pulmonary scintigraphy or autopsy, sensitivity of TEE for diagnosis of massive pulmonary embolism (MPE) in patients with right ventricular dilatation was 92%; and specificity was 100%;. In patients without right ventricular dilatation, left ventricular dysfunction (four patients) or cardiac tamponade (two patients) was confirmed. Intrapulmonary thrombolysis was evaluated in 11 of 13 patients with MPE. Two patients died prior to attempted thrombolysis. Three patients received streptokinase and eight received urokinase. Twenty-four hours after beginning of treatment, total pulmonary resistance index significantly decreased for 59%; and mean pulmonary artery pressure for 31%;. Cardiac index increased for 74%;. Nine of 11 patients receiving thrombolysis survived to hospital discharge. Conclusion Bedside TEE is a valuable tool for diagnosis of MPE. It enables immediate intrapulmonary thrombolysis, which seems to be an effective therapeutic alternative in our group of patients with obstructive shock.

In the current operation of automated external defibrillators, substantial time may be consumed for a "hands off" interval during which precordial compression is discontinued to allow for automated rhythm analyses before delivery of the electric countershock. The effects of such a pause on the outcomes of cardiopulmonary resuscitation were investigated.Prospective, randomized, controlled animal study.Research laboratory.Male Sprague-Dawley rats.Ventricular fibrillation was electrically induced in 25 Sprague-Dawley rats. After 4 mins of untreated ventricular fibrillation, precordial compression was begun and continued for 6 mins. Animals were then randomized to receive an immediate defibrillation shock or the defibrillation attempt was delayed for intervals of 10, 20, 30, or 40 secs.Immediate defibrillation restored spontaneous circulation in each instance. When defibrillation was delayed for 10 or 20 secs, spontaneous circulation was restored in three of five animals in each group. After a 30-sec delay, spontaneous circulation was restored in only one of five animals (p.05). No animal was successfully resuscitated after a 40-sec delay (p.01). With increasing delays, 24- and 48-hr survival rates were correspondingly reduced.During resuscitation from ventricular fibrillation, prolongation of the interval between discontinuation of precordial compression and delivery of the first electric countershock substantially compromises the success of cardiac resuscitation. Accordingly, automated defibrillators are likely to be maximally effective if they are programmed to secure minimal "hands off" delay before delivery of the electric countershock.

Patients with sudden cardiac arrest who regain consciousness after ROSC should undergo immediate coronary angiography unless obvious non-coronary cause is identified. Revascularization strategy should follow the guidelines for acute coronary syndromes and stable coronary disease for patients without preceding cardiac arrest. In comatose survivors of cardiac arrest, immediate coronary angiography should be performed if there is no obvious non-coronary cause and there is realistic hope for neurological recovery. Due to uncertain neurological outcome, immediate percutaneous revascularization should be focused on obvious acute thrombotic lesions followed by staged intervention if patient wakes from the coma.

The aim of this study was to confirm the cardioprotective effects of hypothermia using a combination of cold saline and endovascular cooling.Hypothermia has been reported to reduce infarct size (IS) in patients with ST-segment elevation myocardial infarctions.In a multicenter study, 120 patients with ST-segment elevation myocardial infarctions (6 h) scheduled to undergo percutaneous coronary intervention were randomized to hypothermia induced by the rapid infusion of 600 to 2,000 ml cold saline and endovascular cooling or standard of care. Hypothermia was initiated before percutaneous coronary intervention and continued for 1 h after reperfusion. The primary end point was IS as a percent of myocardium at risk (MaR), assessed by cardiac magnetic resonance imaging at 4 ± 2 days.Mean times from symptom onset to randomization were 129 ± 56 min in patients receiving hypothermia and 132 ± 64 min in controls. Patients randomized to hypothermia achieved a core body temperature of 34.7°C before reperfusion, with a 9-min longer door-to-balloon time. Median IS/MaR was not significantly reduced (hypothermia: 40.5% [interquartile range: 29.3% to 57.8%; control: 46.6% [interquartile range: 37.8% to 63.4%]; relative reduction 13%; p = 0.15). The incidence of heart failure was lower with hypothermia at 45 ± 15 days (3% vs. 14%, p 0.05), with no mortality. Exploratory analysis of early anterior infarctions (0 to 4 h) found a reduction in IS/MaR of 33% (p 0.05) and an absolute reduction of IS/left ventricular volume of 6.2% (p = 0.15).Hypothermia induced by cold saline and endovascular cooling was feasible and safe, and it rapidly reduced core temperature with minor reperfusion delay. The primary end point of IS/MaR was not significantly reduced. Lower incidence of heart failure and a possible effect in patients with early anterior ST-segment elevation myocardial infarctions need confirmation. (Efficacy of Endovascular Catheter Cooling Combined With Cold Saline for the Treatment of Acute Myocardial Infarction [CHILL-MI]; NCT01379261).

BACKGROUND Primary angioplasty has been shown to be superior to thrombolysis. However, previous reports have shown a negative impact of longer time-to-treatment on myocardial perfusion and survival even with mechanical reperfusion. However, these deleterious effects might potentially be overcome by an extensive use of glycoprotein (Gp) IIb-IIIa inhibitors. Thus, the aim of the current study was to evaluate the prognostic role of the interval from symptoms onset to reperfusion in a large cohort of patients undergoing primary angioplasty with Gp IIb-IIIa inhibitors. METHODS Our population is represented by 1560 patients undergoing primary angioplasty for ST-segment elevation myocardial infarction (STEMI) included in the EGYPT (Early Glycoprotein IIb-IIIa Inhibitors in Primary Angiography) database. Myocardial perfusion was evaluated by angiography or ST-segment resolution, whereas infarct size was estimated by using peak creatine kinase and creatine kinase-MB (CK-MB). Follow-up data were collected between 30 days and 1 year after primary angioplasty. RESULTS Time-to-treatment was significantly associated with age and female sex, diabetes and previous myocardial infarction (MI), but inversely related to smoking. Time-to-treatment affected the rate of postprocedural thrombolysis in myocardial infarction (TIMI) 3 flow (P

Hypertension is a well-known risk factor for atherosclerosis. However, data on the impact of hypertension in patients with ST elevation myocardial infarction (STEMI) are inconsistent and mainly related to studies performed in the thrombolytic era, with very few data on patients undergoing primary angioplasty. The aim of the present study was to evaluate the impact of hypertension on distal embolization, myocardial perfusion, and mortality in patients with STEMI undergoing primary percutaneous coronary intervention. Our population is represented by 1,662 patients undergoing primary angioplasty for STEMI included in the Early Glycoprotein IIb-IIIa inhibitors in Primary angioplasty database. Myocardial perfusion was evaluated by myocardial blush grade and ST segment resolution. Follow-up data were collected within 1 year after primary angioplasty. Hypertension was observed in 700 patients (42.1%). Hypertension was associated with more advanced age (p 0.001), female gender (p0.001), diabetes (p0.001), hypercholesterolemia (p0.001), previous revascularization (p0.001), anterior myocardial infarction (p = 0.006), longer ischemia time (p = 0.03), more extensive coronary artery disease (p = 0.002), more often treated with abciximab (p0.001), and less often smokers (p0.001). Hypertension was associated with impaired postprocedural myocardial blush grade 2 to 3 (68.2% vs 74.2%, p = 0.019) and complete ST segment resolution (51.7% vs 61.1%, p = 0.001). By a mean follow-up of 206 ± 158 days, 70 patients (4.3%) had died. Hypertension was associated with a greater mortality (6.2% vs 2.9%, hazard ratio 2.31, 95% confidence interval 1.42 to 3.73, p 0.001), confirmed after correction for baseline confounding factors (hazard ratio 1.82, 95% confidence interval 1.03 to 3.22, p0.001). In conclusion, this study showed that among patients with STEMI undergoing primary angioplasty, hypertension is associated with impaired reperfusion and independently predicts 1-year mortality.

Summary Background Although primary angioplasty achieves thrombolysis in myocardial infarction (TIMI) 3 flow in most patients with ST-elevation myocardial infarction, epicardial recanalization does not guarantee optimal perfusion in a large proportion of patients. The influence of multivessel disease on myocardial reperfusion and survival after primary angioplasty has not been extensively investigated. Aim To evaluate the impact of multivessel disease on myocardial perfusion and survival in a large cohort of patients with ST-elevation myocardial infarction treated with angioplasty and glycoprotein (GP) IIb/IIIa inhibitors. Methods This analysis is based on 1494 patients undergoing primary angioplasty included in the EGYPT database. Myocardial perfusion was evaluated by angiography or ST-segment resolution, whereas infarct size was estimated by using peak creatine kinase-MB (CK-MB). Follow-up data were collected between 30 days and 1 year after primary angioplasty. Results Multivessel disease was observed in 870 patients (58.2%). The extent of coronary artery disease was associated with age, diabetes, hypertension, previous myocardial infarction, previous revascularization, abciximab treatment and longer ischaemic time, and was independently associated with impaired angiographic myocardial perfusion (adjusted odds ratio 1.18, 95% confidence interval [CI] 1.01–1.40, P = 0.049). At 208 ± 160 days, the extent of coronary artery disease was independently associated with higher mortality (adjusted hazard ratio 1.54, 95% CI 1.06–2.24, P = 0.022). Conclusions Among patients with ST-elevation myocardial infarction undergoing primary angioplasty with GP IIb/IIIa inhibitor treatment, the extent of coronary artery disease was independently associated with impaired myocardial perfusion and survival.

AIMS Considerable interest has been focused in recent years on the role of distal embolisation as a major determinant of impaired reperfusion after primary angioplasty for STEMI. The aim of the current study was to evaluate in a large cohort of STEMI patients undergoing primary angioplasty with glycoprotein (Gp) IIb-IIIa inhibitors, whether the impact of distal embolisation on myocardial perfusion and survival may depend on time-to-treatment. METHODS AND RESULTS Our population is represented by 1,182 patients undergoing primary angioplasty for STEMI included in the EGYPT database. Patients were grouped according to time-to-treatment ( 6 hours). Distal embolisation was defined as an abrupt "cutoff" in the main vessel or one of the coronary branches of the infarct-related artery, distal to the angioplasty site. Myocardial perfusion was evaluated by angiography or ST-segment resolution, whereas infarct size was estimated by using peak creatine kinase (CK) and CK-MB. Follow-up data were collected between 30 days and one year after primary angioplasty. Distal embolisation was observed in 132 patients (11.1%) and tended to occur more frequently in late presenters (p=0.067). Patients with distal embolisation less often had post-procedural Thrombolysis In Myocardial Infarction (TIMI) 3 flow (p

Despite optimal epicardial recanalization, primary angioplasty for ST-elevation myocardial infarction (STEMI) is still associated with suboptimal reperfusion in a relatively large proportion of patients. The aim of the current study was to evaluate the impact of preprocedural TIMI flow on myocardial perfusion, distal embolization, and survival among STEMI patients undergoing primary angioplasty with glycoprotein (GP) IIb/IIIa inhibitors.Our population is represented by a total of 1637 patients undergoing primary angioplasty for STEMI treated with GP IIb/IIIa inhibitors. Myocardial perfusion was evaluated by myocardial blush grade and ST-segment resolution. Follow-up data were collected between 30 days and 1 year after primary angioplasty.Poor preprocedural TIMI flow (TIMI 0-1) was observed in 1039 patients (63.5%), and was associated with higher Killip class at presentation (P=.006), longer time-to-treatment (P=.03), less often with early administration of GP IIb/IIIa inhibitors (P.001), impaired postprocedural epicardial (P=.001) and myocardial perfusion (determined by myocardial blush grade, P.001 and/or ST-segment resolution (P.001), and distal embolization (P=.041). At 206 ± 158 days follow-up, poor preprocedural recanalization was associated with a significantly higher mortality (adjusted odds ratio, 0.58; 95% CI, 0.34-0.96; P=.034).This study shows that among patients with STEMI undergoing primary angioplasty with GP IIb/IIIa inhibitors, poor preprocedural TIMI flow is associated with higher incidence of distal embolization and impaired epicardial and myocardial perfusion, and significantly higher mortality.

To evaluate the effect of spontaneous gasping on cardiorespiratory functions and the ability to resuscitate during experimental cardiac arrest.Studies in rat and pig models during cardiac arrest and cardiopulmonary resuscitation (CPR).We retrospectively examined the role of spontaneous gasping during the course of experimental studies on cardiopulmonary resuscitation.The data were extracted to illustrate the mechanisms of spontaneous gasping and its effects on pulmonary gas exchange and blood circulation during CPR.Spontaneous gasping increased PaO2 and decreased PaCO2 values during precordial compression in the absence of mechanical ventilation. The frequency of gasping during precordial compression was greater in successfully resuscitated animals. A significant linear correlation was established between coronary artery perfusion pressure and both the frequency (r2 = .90, p.01) and the duration (r2 = 0.69, p.01) of gasping during untreated ventricular fibrillation and before resuscitation was attempted. Like coronary perfusion pressure, the frequency and duration of gasping predicted the success of cardiac resuscitation attempts.Spontaneous gasping is associated with both pulmonary and hemodynamic effects during cardiac arrest in experimental animals. Spontaneous gasping is biologically useful and is predictive of a more favorable outcome of resuscitative efforts.

Extracorporeal life support (ELS) is emerging as a standard treatment option for acute respiratory and/or cardiac failure. In this article we describe our first year of experience with ELS activity in adult medical patients in our center. Veno-venous extracorporeal membrane oxygenation (VV ECMO) support was applied in cases of severe acute respiratory distress syndrome (ARDS) not responsive to conventional treatments. The use of veno-arterial (VA) ECMO support was reserved for cases of cardiac shock refractory to standard treatment and cardiac arrests not responding to conventional resuscitation. A total of 19 patients were treated with ELS during the first year of activity. Eight of these received VV ECMO for ARDS of various etiologies, with a survival rate of 63%. Eleven patients received VA ECMO support due to cardiac failure (2 post-resuscitation). Survival in this group was 45%. We report our results, including complications and organizational issues that we encountered, and describe protocol improvements developed over the short period of time since ELS treatment has been implemented in our center.

Summary. Background: Even although time to treatment has been shown to be a determinant of mortality in primary angioplasty, the potential benefits are still unclear from early pharmacological reperfusion by glycoprotein (Gp) IIb-IIIa inhibitors. Therefore, the aim of this meta-analysis was to combine individual data from all randomized trials conducted on upstream as compared with late peri-procedural abciximab administration in primary angioplasty. Methods: The literature was scanned using formal searches of electronic databases (MEDLINE and EMBASE) from January 1990 to December 2010. All randomized trials on upstream abciximab administration in primary angioplasty were examined. No language restrictions were enforced. Results: We included a total of seven randomized trials enrolling 722 patients, who were randomized to early (n = 357, 49.4%) or late (n = 365, 50.6%) peri-procedural abciximab administration. No difference in baseline characteristics was observed between the two groups. Follow-up data were collected at a median (25th–75th percentiles) of 1095 days (720–1967). Early abciximab was associated with a significant reduction in mortality (primary endpoint) [20% vs. 24.6%; hazard ratio (HR) 95% confidence interval (CI) = 0.65 (0.42–0.98) P = 0.02, Phet = 0.6]. Furthermore, early abciximab administration was associated with a significant improvement in pre-procedural thrombolysis in myocardial infarction (TIMI) 3 flow (21.6% vs. 10.1%, P

QTc interval and left ventricular regional wall motion abnormality score (WMS) were assessed in 61 consecutive patients with 4-day-old acute myocardial infarction (AMI). There were 45 men and 16 women, aged 60.6 +/- 8.7 years; 24 had anterior wall AMI and 37 had inferior wall AMI. Twenty-nine patients received thrombolytic treatment, which was presumably successful in 19. The longest QTc interval from a standard 12-lead electrocardiogram, corrected by Bazett's formula, was considered for the study. The WMS was evaluated echocardiographically. The authors found a statistically significant correlation between WMS and QTc interval duration; the correlation was stronger in patients with anterior AMI (r = .9, P.001) than in those with inferior AMI (r = .66, P.001). The WMS and QTc values were significantly lower in patients with successful thrombolytic treatment compared to those with unsuccessful thrombolysis (P.003 and P.002, respectively). The authors could demonstrate no significant correlation between serum potassium concentration and the QTc interval. In patients with anterior AMI, QTc interval duration might represent an additional marker of left ventricular systolic dysfunction. It could also be used as an additional noninvasive criterion of coronary artery reperfusion in patients with AMI.

Manual catheter aspiration appears to be a useful adjunct to primary percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction. We investigated effects of catheter aspiration during primary PCI in patients with different extents of coronary thrombus. The study included 46 patients with no or possible thrombus (thrombus scale [TS] grades 0 to 1) and 135 patients with angiographic evidence of obvious thrombus (TS grades 2 to 5). Reference vessel diameter, which was significantly larger in the group with TS grades 2 to 5 (3.4 vs 3.2 mm, p = 0.004), was the only independent predictor of angiographically visible thrombus (odds ratio 3.3, 95% confidence interval 1.3 to 8.7, p = 0.015, per millimeter increase). Aspiration catheter was successfully advanced across the lesion in 89% of patients with TS grades 0 to 1 and 96% of those with TS grades 2 to 5 (p = 0.115). Number of aspirations varied from 1 to 5 and was significantly larger in patients with TS grades 2 to 5. Visually observable aspirate was obtained in 90% of patients with TS grades 2 to 5 and in 67% of patients with TS grades 0 to 1 (p0.001) with more patients with TS grades 2 to 5 having aspirate5 mm in length (49% vs 11%, p0.001). Final Thrombolysis In Myocardial Infarction grade 3 flow (89% vs 92%), residual TS (0.2 vs 0.1), frequency of distal embolization (2% vs 6%), and early complete ST resolution (65% vs 70%) were comparable between groups with TS grades 0 to 1 and 2 to 5. In conclusion, although the amount of aspirate is larger in patients with angiographically obvious thrombus, visually observable aspirate can be obtained in most patients without definite signs of thrombus. Extent of coronary thrombus does not influence primary PCI result if manual aspiration is used.

Because an acute coronary thrombotic event may be viewed as the main trigger of sudden cardiac arrest, urgent coronary angiography followed by percutaneous coronary intervention appeared as a promising tool in the early postresuscitation phase. Unfortunately, large randomized trials, which have unequivocally demonstrated benefits of urgent percutaneous coronary intervention in patients with acute coronary syndromes, systematically excluded patients with preceding cardiac arrest followed by successful reestablishment of spontaneous circulation. There are several nonrandomized trials in patients with electrocardiographic signs of acute ST-elevation myocardial infarction after reestablishment of spontaneous circulation which together accumulated 478 patients. After urgent coronary angiography, percutaneous coronary intervention was performed in 98%. Patency of infarct-related artery was reestablished in 89%. Success of primary percutaneous coronary intervention and hospital survival in patients regaining consciousness soon after reestablishment of spontaneous circulation appeared to be comparable with ST-elevation myocardial infarction population without preceding cardiac arrest. This is in contrast with comatose survivors of cardiac arrest in whom survival to hospital discharge was, despite somewhat smaller patency of infarct-related artery after percutaneous coronary intervention (94% vs. 82%; p = .12), disproportionably decreased to 57% with good neurologic outcome in only 38%. There is evidence that in these patients, urgent coronary angiography and percutaneous coronary intervention can be safely combined with mild induced hypothermia to facilitate neurologic recovery.

Urgent invasive coronary strategy including coronary angiography and percutaneous coronary intervention (PCI) is feasible and safe in combination with mild induced hypothermia and may significantly improve survival with good neurological outcome in comatose patients after reestablishment of spontaneous circulation (ROSC). The starting hypothermia already in the prehospital setting or immediately after arrival to the catheterization laboratory to complement urgent coronary angi-ography and PCI seems to be a logical strategy.

Background Although primary angioplasty has been shown to improve survival as compared with thrombolysis, the outcome is still unsatisfactory in subsets of patients such as those with signs of heart failure at presentation. In fact, although primary angioplasty is able to restore TIMI 3 flow in most patients, suboptimal myocardial reperfusion is observed in a relatively large proportion of patients. The aim of this study was to investigate among patients with ST-segment elevation myocardial infarction undergoing primary angioplasty the association between heart failure at presentation and myocardial perfusion and its implications in terms of survival. Methods Our population is represented by patients undergoing primary angioplasty who are included in the EGYPT database. Congestive heart failure was defined as Killip class >1 at admission. Myocardial perfusion was evaluated by myocardial blush grade and ST-segment resolution. Follow-up data were collected between 30 days and 1 year after primary angioplasty. Results Detailed data on Killip class at presentation were available in 1,427 of 1,662 patients (86% of the initial population) who represent the final population of this study. Killip class was associated with myocardial perfusion, distal embolization, enzymatic infarct size, predischarge ejection fraction, and 1-year mortality rate. Myocardial blush was an independent predictor of 1-year mortality (hazard ratio 7.44, 95% CI 1.82-30.4, P = .005) in patients with advanced Killip class at presentation. Conclusions Our study shows that patients with heart failure complicating ST-segment elevation myocardial infarction have impaired myocardial perfusion, which accounts for the poor outcome observed in these patients. Further efforts should be aimed at improving myocardial perfusion, beyond epicardial recanalization, to further improve the outcome of these high-risk patients.

It has been shown that, among patients with ST-segment elevation myocardial infarction (STEMI), diabetes is associated with a significantly higher mortality. The aim of the current study was to investigate the impact of diabetes on myocardial perfusion and mortality among STEMI patients treated with primary angioplasty and glycoprotein IIb-IIIa inhibitors.Our population is represented by a total of 1662 patients undergoing primary angioplasty for STEMI included in 11 randomized trials. Myocardial perfusion was evaluated by angiography (n=1324) or postprocedural ECG (n=1371). Distal embolization was defined as an abrupt "cutoff" in the main vessel or one of the coronary branches of the infarct-related artery, distal to the angioplasty site (data available in 1181 patients).Diabetes was observed in a total of 281 patients (16.9%). Diabetic patients were older, with a larger prevalence of female gender, hypertension, hypercholesterolemia, advanced killip class at presentation and multivessel disease. Diabetes was associated with impaired postprocedural TIMI 3 flow (82% vs 90%, p0.001), MBG 2-3 (60.1% vs 74.2%, p0.001), complete ST-segment resolution (43.2% vs 60%, p0.001) and more distal embolization (16.4% vs 10.1%, p0.0001). The association with impaired MBG and distal embolization was confirmed after correction for baseline confounding factors. Diabetes was associated with significantly impaired mortality (12.6% vs 3.9%, HR=3.0 [1.84-4.89], p0.001), that persisted even after correction for baseline confounding factors (HR=2.6 [1.52-4.45], p=0.001).This study showed that, among patients with STEMI undergoing primary angioplasty on the top of glycoprotein IIb-IIIa inhibitors, diabetes mellitus is independently associated with impaired perfusion and distal embolization, that contribute to explain the higher mortality observed in these patients.

The Early Glycoprotein IIb-IIIa inhibitors in Primary angioplasty (EGYPT) cooperation aimed at evaluating, by pooling individual patient’s data of randomized trials, the benefits of pharmacological facilitation with Gp IIb-IIIa inhibitors among STEMI patients undergoing primary angioplasty. In the current study we analyze the benefits of early Gp IIb-IIIa inhibitors in diabetic patients. The literature was scanned by formal searches of electronic databases (MEDLINE, EMBASE) from January 1990 to October 2007. We examined all randomized trials on facilitation by early administration of Gp IIb-IIIa inhibitors in STEMI. No language restrictions were enforced. Individual patients’ data were obtained from 11 out of 13 trials, including 1,662 patients. Diabetes was present in 281 (16.9%). Early Gp IIb-IIIa inhibitors were associated with improved preprocedural TIMI 3 flow (26.0% vs. 13.1%, P = 0.006), postprocedural TIMI 3 flow (90.1% vs. 75.0%, P = 0.18), MBG 3 (40.8% vs. 30.4%, P = 0.004), and less distal embolization (11.6% vs. 20.8%, P = 0.05). However, early Gp IIb-IIIa inhibitors did not significantly reduce mortality (8.3% vs. 9.5%, P = 0.64). This meta-analysis shows that pharmacological facilitation with early administration of Gp IIb-IIIa inhibitors in STEMI patients with diabetes undergoing primary angioplasty, is associated with significant benefits in terms of preprocedural and postprocedural TIMI flow, improved myocardial perfusion, without significant benefits in mortality.

A 17-year-old previously healthy girl with profound circulatory shock following a heroin overdose is reported. Except for opiates no other substances and specifically no cocaine were found in the blood and urine samples. Even though the mechanism of shock is not completely understood, severe depression of left ventricular contractility seems to be the predominant reason. Acute right heart failure with decreased pulmonary capillary wedge pressure and arterial vasodilatation resulting in maldistribution of cardiac output cannot be ruled out as possible contributing factors. The shock was successfully reversed with volume loading and a high dose of dobutamine. The recovery was uneventful and the patient was discharged with normal cardiac function.

After successful cardiopulmonary resuscitation, acute ST-elevation myocardial infarction (STEMI) may be documented. We investigated the incidence and prognosis of patients admitted to our department between 1 January 2000 and 31 December 2004. Among 2393 consecutive patients with STEMI, 135 (5.7%) presented after a return of spontaneous circulation (ROSC). Forty-nine patients (36%) regained consciousness and 86 patients (64%) remained unconscious during initial evaluation. The delay from collapse to advanced cardiac life support (ACLS) was longer in comatose patients (5.8 min versus 0.5 min; p

Carbon monoxide (CO) poisoning is the most common form of lethal poisoning. The aim of this prospective clinical study was to assess the possible role of S100B, the structural protein in the astroglia, as a biochemical marker of brain injury in carbon monoxide poisoning. Serum S100B determination was performed in 38 consecutive patients poisoned by carbon monoxide who were admitted to the Emergency Department (ED) in Ljubljana. All three unconscious patients had elevated S100B levels. The patient with the highest S100B died. S100B was elevated in two of the six patients with initial transitory unconsciousness at the scene. All 29 patients without loss of consciousness had normal S100B levels. Carbon monoxide poisoning appears to be associated with elevated S100B levels.

Background: Patients infected with human immunodeficiency virus (HIV) are at an increased risk for premature coronary artery disease. However, the clinical outcome of HIV-infected patients who have had an acute myocardial infarction (AMI) is unknown. Methods: We studied 24 consecutive HIV-infected patients admitted because of AMI. During the hospital phase, the patients were examined for recurrent ischemia, congestive heart failure, arrhythmia, and death. Patients were followed up for an average of 15 months after discharge for reinfarction; recurrent angina; the need for any angioplasty, bypass surgery, or target vessel revascularization for restenosis and stent thrombosis; HIV-related complications; and death. For comparison, we included a matched control group of non– HIV-infected patients. Results: The HIV-infected patients with AMI were predominantly male (21 [88%]), 47 ±9 years of age. Twenty-two (92%) were receiving antiretroviral treatment; 17 (71%), protease inhibitors; and 13 (54%), lipidlowering therapy. With aggressive therapy, the lipid profile was similar in HIV-infected patients treated with protease inhibitors and those who were not. Twentyone (88%) of 24 patients underwent immediate angiography and 20 (83%) had angioplasty or bypass surgery. The HIV-infected patients with AMI had a benign in-hospital course, with no deaths or reinfarction. The admission characteristics, treatment strategy, and inhospital outcome were similar in the matched uninfected patients with AMI. After discharge, HIV-infected patients had a higher incidence of reinfarction (4/20 [20%] vs 2/45 [4%]; P=.07), and 6 (43%) of 14 HIV-infected patients who had successful percutaneous coronary intervention and were available for follow-up required target vessel revascularization compared with 4 (11%) of 38 uninfected patients who had successful percutaneous coronary intervention and were available for follow-up (P=.02). Conclusions: Patients infected with HIV sustain AMI at a young age and have a benign in-hospital course. Although HIV-infected patients have a higher incidence of postdischarge ischemic events, restenosis, and stent thrombosis, the intermediate-term mortality is low. Arch Intern Med. 2003;163:457-460

Risk stratification in patients with unstable angina remains a challenging task. Troponins, electrocardiographic changes and clinical characteristics are the most widely employed parameters. Blood pressure and heart rate are proven predictors of short-term outcome; no study, however, has investigated the dynamics of these variables. We postulated that measurements of these parameters performed at the beginning of an ischemic episode would reflect the extent of coronary disease and would predict short-term outcome.Analysis of variance and multivariate logistic regression were used to analyze the relationship of systolic blood pressure and heart rate during ischemic episodes with the occurrence of adverse ischemic events (death, infarction, need for revascularization) prior to hospital discharge.In a group of 193 patients mortality rate was 4.2%, infarction rate 8.4% and revascularization rate 42.4%. Systolic blood pressure increased during ischemic episodes compared to baseline values in the group of survivors (p0.0001), while there were no significant changes in the group of non-survivors. The rise in heart rate during ischemic episodes was greater in non-survivors, even though significant changes were observed in both groups. Systolic pressure and heart rate were independent predictors of mortality (p = 0.01 and p = 0.003, respectively), but were not predictive of infarction or revascularization.Low systolic blood pressure and high heart rate at the beginning of an ischemic episode predict higher in-hospital mortality in patients with unstable angina. Clinical presentation during the ischemic episode should be considered in risk stratification.

Acute myocardial infarction induces an inflammatory reaction. We related conventional inflammatory parameters including C-reactive protein, erythrocyte sedimentation rate, white blood cell count and axillary temperature to plasma concentrations of procalcitonin in patients with acute myocardial infarction. In a prospective-descriptive study, we evaluated 54 patients with acute myocardial infarction. During a time period of 8 days following myocardial infarction, C-reactive protein, erythrocyte sedimentation rate, white blood cell count and axillary temperature as well as the plasma concentrations of procalcitonin were measured. Maximal procalcitonin remained normal (below 0.5 microgram/L) in patients with uncomplicated acute myocardial infarction. This contrasted with results obtained from patients additionally afflicted by pulmonary edema and cardiogenic shock, in whom maximal procalcitonin increased up to 5.24 micrograms/L. Resuscitation after cardiac arrest and/or concomitant bacterial infection increased procalcitonin to a maximal value of 134 micrograms/L, which was independent of the severity of left heart failure. Conventional inflammatory parameters were all significantly increased even in the absence of cardiac and non-cardiac complications of acute myocardial infarction. In conclusion, procalcitonin increases in patients with acute myocardial infarction only if associated with severe left heart failure, resuscitation after cardiac arrest or in the presence of bacterial infections. Thus, procalcitonin may help to elucidate the etiology of systemic inflammatory response during the early course of acute myocardial infarction.

Objective Inhalation of helium, which produces a change in the voice, is frequently used among young rock singers to improve their performance. Design A case report. Settings Adult medical intensive care unit in a university hospital. Patient A 23-yr-old singer, who accidentally inhaled helium from a high pressurized tank without pressure reduction, presented with transient loss of consciousness and chest pain. Interventions Electrocardiogram, chest radiograph, biochemical and toxicological analyses, echocardiography, coronary angiography were performed. Measurements and Main Results At admission, the patient slowly regained consciousness. An electrocardiogram showed significant ST elevations in leads I, aVL, and V4–V6. The chest radiograph was consistent with pulmonary congestion and pneumomediastinum. The echocardiogram showed normal sized heart chambers with hypokinesis of the left ventricular lateral wall. Ethanol and urine cannabinoids were present in low concentrations, but no presence of opiates, methadone, cocaine, or amphetamines was documented. Troponin T was positive. Elevation of ST segments gradually disappeared within 30 mins, the drowsiness within 10 hrs, and the thoracic pain within 24 hrs. Coronary angiography showed normal coronary arteries. The patient was discharged on day 3 without any symptoms and with normal electrocardiogram and chest radiograph. Conclusion Accidental inhalation of helium under high pressure can cause symptomatic cerebral and coronary artery gas embolism.

Coronary artery disease is the most frequent cause of sudden cardiac death. There is general consensus that immediate coronary angiography with percutaneous coronary intervention (PCI) should be performed in all conscious and unconscious patients with ST-elevation myocardial infarction in post-resuscitation electrocardiogram. In these patients acute coronary thrombotic lesion (“ACS” lesion) suitable for PCI is typically present in more than 90%. PCI in these patients is not only feasible and safe but highly effective and there is evidence of improved survival with good neurological outcome. PCI of the culprit lesion is the primary goal while PCI of stable obstructive lesions may be postponed unless post-resuscitation cardiogenic shock is present.

Spontaneous coronary artery dissection is an extremely rare cause of myocardial infarction. The prognosis and treatment of coronary artery dissection have not yet been defined. We report on a 42-year-old woman who was admitted to the emergency unit of a regional hospital with central chest pain and electrocardiographic signs of extensive acute anterior myocardial infarction (MI). She was treated with thrombolytics, yet her condition deteriorated rapidly, resulting in cardiogenic shock. An angiogram revealed dissection of the left main coronary artery that extended into the anterior descending (LAD) and circumflex arteries (LCX). At autopsy a recent anterolateral MI of the left ventricle was found. Dissection of the left coronary artery system was confirmed. Extension of the dissection may have been due to thrombolytic treatment. Cathet Cardiovasc Intervent 2001;52:226–230. © 2001 Wiley-Liss, Inc.

Objective To describe rare side effects of treatment with isoniazid. Design Descriptive case report. Setting Medical intensive care unit in a university medical center. Patient A 14-yr old previously healthy girl receiving preventive isoniazid therapy who suddenly developed generalized tonic-clonic seizures and coma. Interventions Patient was sedated and mechanically ventilated. She also received pyridoxine intravenously. Measurements and main results An isoniazid overdose was not confirmed. Computed tomography of the brain and electroencephalogram revealed nothing abnormal. Seizures gradually disappeared within 2 hrs after sedation and treatment with pyridoxine. The patient was discharged on day 14 without consequences and has been well for 10 mos. No seizures reappeared after isoniazid was discontinued. Conclusions We caution against possible isoniazid neurotoxicity in healthy individuals using recommended preventive doses.

Objectives: To identify a method for predicting the success or failure of a defibrillatory shock such as to avoid potentially detrimental interruptions of cardiopulmonary resuscitation (CPR). Such a method would also guide more optimal programming of automated external defibrillators. Design: Prospective, observational animal study. Setting: Medical research laboratory in a university-affiliated research and educational foundation. Subjects: Domestic pigs. Interventions: Ventricular fibrillation (VF) was electrically induced in 66 domestic pigs. After an interval of between 3 and 5 mins of untreated VF, precordial compression was begun. Electrocardiographic lead 2 was monitored and artifacts produced during precordial compression were removed by digital filtering. Measurements and Main Results: In the derivation study, electrical defibrillation restored spontaneous circulation in 30 of the 66 animals. Successfully resuscitated animals had significantly greater coronary perfusion pressure, maximum VF amplitude, mean VF amplitude, and dominant VF frequency. No animals were resuscitated if the coronary perfusion pressure was

Background In a rodent model of cardiac arrest and resuscitation in which the inspired gas mixture was enriched with oxygen, resuscitability and survival were unaffected by positive pressure ventilation. In the present study, in a larger animal model, tidal volumes generated during precordial compression and with spontaneous gasping were quantitated. Methods Domestic pigs with an average weight of 34 kg were anesthetized with pentobarbital. Ventricular fibrillation (VF) was induced electrically. Precordial compression was begun after 4 min of untreated VF. Each of 22 animals received one of two interventions in conjunction with precordial compression: positive pressure ventilation with oxygen or oxygen supplied at the port of a tracheal tube at ambient pressure. After 8 min of precordial compression, defibrillation was attempted. Results Only very moderate increases in arterial Pco2 were documented during cardiopulmonary resuscitation in the absence of mechanical ventilation but arterial oxygen tension was consistently in excess of 100 mm Hg. Cardiac resuscitability and 48-h survival were approximately the same in animals maintained on inspired oxygen whether or not they were mechanically ventilated (7/11 or 8/11). In the absence of mechanical ventilation, precordial compression and spontaneous gasping yielded minute volumes that exceeded 5 L. Conclusion Positive pressure mechanical ventilation did not improve resuscitability or postresuscitation outcome in this porcine model of cardiac arrest.