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Objective: Serum troponin concentrations predict mortality in almost every clinical setting they have been examined, including sepsis. However, the causes for troponin elevations in sepsis are poorly understood. We hypothesized that detailed investigation of myocardial dysfunction by echocardiography can provide insight into the possible causes of troponin elevation and its association with mortality in sepsis., Design: Prospective, analytic cohort study., Setting: Tertiary academic institute., Patients: A cohort of ICU patients with severe sepsis or septic shock., Interventions: Advanced echocardiography using global strain, strain-rate imaging and 3D left and right ventricular volume analyses in addition to the standard echocardiography, and concomitant high-sensitivity troponin-T measurement in patients with severe sepsis or septic shock., Measurements and Main Results: Two hundred twenty-five echocardiograms and concomitant high-sensitivity troponin-T measurements were performed in a cohort of 106 patients within the first days of severe sepsis or septic shock (2.1 ± 1.4 measurements/patient). Combining echocardiographic and clinical variables, left ventricular diastolic dysfunction defined as increased mitral E-to-strain-rate e'-wave ratio, right ventricular dilatation (increased right ventricular end-systolic volume index), high Acute Physiology and Chronic Health Evaluation-II score, and low glomerular filtration rate best correlated with elevated log-transformed concomitant high-sensitivity troponin-T concentrations (mixed linear model: t = 3.8, 3.3, 2.8, and -2.1 and p = 0.001, 0.0002, 0.006, and 0.007, respectively). Left ventricular systolic dysfunction determined by reduced strain-rate s'-wave or low ejection fraction did not significantly correlate with log(concomitant high-sensitivity troponin-T). Forty-one patients (39%) died in-hospital. Right ventricular end-systolic volume index and left ventricular strain-rate e'-wave predicted in-hospital mortality, independent of Acute Physiology and Chronic Health Evaluation-II score (logistic regression: Wald = 8.4, 6.6, and 9.8 and p = 0.004, 0.010, and 0.001, respectively). Concomitant high-sensitivity troponin-T predicted mortality in univariate analysis (Wald = 8.4; p = 0.004), but not when combined with right ventricular end-systolic volume index and strain-rate e'-wave in the multivariate analysis (Wald = 2.3, 4.6, and 6.2 and p = 0.13, 0.032, and 0.012, respectively)., Conclusions: Left ventricular diastolic dysfunction and right ventricular dilatation are the echocardiographic variables correlating best with concomitant high-sensitivity troponin-T concentrations. Left ventricular diastolic and right ventricular systolic dysfunction seem to explain the association of troponin with mortality in severe sepsis and septic shock.

Rationale: Human genetics have implicated the 5-lipoxygenase enzyme in the pathogenesis of cardiovascular disease, and an inhibitor of the 5-lipoxygenase activating protein (FLAP) is in clinical development for asthma., Objective: Here we determined whether FLAP deletion modifies the response to vascular injury., Methods and Results: Vascular remodeling was characterized 4 weeks after femoral arterial injury in FLAP knockout mice and wild-type controls. Both neointimal hyperplasia and the intima/media ratio of the injured artery were significantly reduced in the FLAP knockouts, whereas endothelial integrity was preserved. Lesional myeloid cells were depleted and vascular smooth muscle cell (VSMC) proliferation, as reflected by bromodeoxyuridine incorporation, was markedly attenuated by FLAP deletion. Inflammatory cytokine release from FLAP knockout macrophages was depressed, and their restricted ability to induce VSMC migration ex vivo was rescued with leukotriene B(4). FLAP deletion restrained injury and attenuated upregulation of the extracellular matrix protein, tenascin C, which affords a scaffold for VSMC migration. Correspondingly, the phenotypic modulation of VSMC to a more synthetic phenotype, reflected by morphological change, loss of α-smooth muscle cell actin, and upregulation of vascular cell adhesion molecule-1 was also suppressed in FLAP knockout mice. Transplantation of FLAP-replete myeloid cells rescued the proliferative response to vascular injury., Conclusions: Expression of lesional FLAP in myeloid cells promotes leukotriene B(4)-dependent VSMC phenotypic modulation, intimal migration, and proliferation.

Prostacyclin (PGI(2)) is a vasodilator and platelet inhibitor, properties consistent with cardioprotection. More than a decade ago, inhibition of cyclooxygenase-2 (COX-2) by the nonsteroidal anti-inflammatory drugs (NSAIDs) rofecoxib and celecoxib was found to reduce the amount of the major metabolite of PGI(2) (PGI-M) in the urine of healthy volunteers. This suggested that NSAIDs might cause adverse cardiovascular events by reducing production of cardioprotective PGI(2). This prediction was based on the assumption that the concentration of PGI-M in urine likely reflected vascular production of PGI(2) and that other cardioprotective mediators, especially nitric oxide (NO), were not able to compensate for the loss of PGI(2). Subsequently, eight placebo-controlled clinical trials showed that NSAIDs that block COX-2 increase adverse cardiovascular events. We connect tissue-specific effects of NSAID action and functional correlates in mice with clinical outcomes in humans by showing that deletion of COX-2 in the mouse vasculature reduces excretion of PGI-M in urine and predisposes the animals to both hypertension and thrombosis. Furthermore, vascular disruption of COX-2 depressed expression of endothelial NO synthase and the consequent release and function of NO. Thus, suppression of PGI(2) formation resulting from deletion of vascular COX-2 is sufficient to explain the cardiovascular hazard from NSAIDs, which is likely to be augmented by secondary mechanisms such as suppression of NO production.

Aims: Systolic dysfunction in septic shock is well recognized and, paradoxically, predicts better outcome. In contrast, diastolic dysfunction is often ignored and its role in determining early mortality from sepsis has not been adequately investigated., Methods and Results: A cohort of 262 intensive care unit patients with severe sepsis or septic shock underwent two echocardiography examinations early in the course of their disease. All clinical, laboratory, and survival data were prospectively collected. Ninety-five (36%) patients died in the hospital. Reduced mitral annular e'-wave was the strongest predictor of mortality, even after adjusting for the APACHE-II score, low urine output, low left ventricular stroke volume index, and lowest oxygen saturation, the other independent predictors of mortality (Cox's proportional hazards: Wald = 21.5, 16.3, 9.91, 7.0 and 6.6, P< 0.0001, <0.0001, 0.002, 0.008, and 0.010, respectively). Patients with systolic dysfunction only (left ventricular ejection fraction ≤50%), diastolic dysfunction only (e'-wave <8 cm/s), or combined systolic and diastolic dysfunction (9.1, 40.4, and 14.1% of the patients, respectively) had higher mortality than those with no diastolic or systolic dysfunction (hazard ratio = 2.9, 6.0, 6.2, P= 0.035, <0.0001, <0.0001, respectively) and had significantly higher serum levels of high-sensitivity troponin-T and N-terminal pro-B-type natriuretic peptide (NT-proBNP). High-sensitivity troponin-T was only minimally elevated, whereas serum levels of NT-proBNP were markedly elevated [median (inter-quartile range): 0.07 (0.02-0.17) ng/mL and 5762 (1001-15 962) pg/mL, respectively], though both predicted mortality even after adjusting for highest creatinine levels (Wald = 5.8, 21.4 and 2.3, P= 0.015, <0.001 and 0.13)., Conclusion: Diastolic dysfunction is common and is a major predictor of mortality in severe sepsis and septic shock.

The endoplasmic reticulum Ca(2+)-sensing STIM proteins mediate Ca(2+) entry signals by coupling to activate plasma membrane Orai channels. We reveal that STIM-Orai coupling is rapidly blocked by hypoxia and the ensuing decrease in cytosolic pH. In smooth muscle cells or HEK293 cells coexpressing STIM1 and Orai1, acute hypoxic conditions rapidly blocked store-operated Ca(2+) entry and the Orai1-mediated Ca(2+) release-activated Ca(2+) current (I(CRAC)). Hypoxia-induced blockade of Ca(2+) entry and I(CRAC) was reversed by NH(4)(+)-induced cytosolic alkalinization. Hypoxia and acidification both blocked I(CRAC) induced by the short STIM1 Orai-activating region. Although hypoxia induced STIM1 translocation into junctions, it did not dissociate the STIM1-Orai1 complex. However, both hypoxia and cytosolic acidosis rapidly decreased Förster resonance energy transfer (FRET) between STIM1-YFP and Orai1-CFP. Thus, although hypoxia promotes STIM1 junctional accumulation, the ensuing acidification functionally uncouples the STIM1-Orai1 complex providing an important mechanism protecting cells from Ca(2+) overload under hypoxic stress conditions.

Purpose of Review: Three topics are at the forefront of the investigation and treatment of patients with coronary artery disease (CAD) undergoing major noncardiac surgery: prophylactic perioperative beta-blockade (PPBB), prophylactic statins and prophylactic preoperative coronary revascularization (PCR). The purpose of the review is to summarize the investigational efforts in each one of these fields and to provide a subjective evaluation as to their impact on perioperative patient care., Recent Findings: The data on PPBB are still controversial. Most recent studies are observational with contradicting results on whether PPBB improves perioperative survival and whether chronic beta-blockade is better than beta-blockers added acutely postoperatively. The data on statins are still evolving and the main question remains whether the proven long-term pleiotrophic, plaque-stabilizing effects of statins translate into measurable improvements in hard outcome in the acute, perioperative setting. The data on PCR are also incomplete. The study that previously reported lack of any perioperative benefit to PCR now provides data that in selected patients PCR may nevertheless improve outcome., Summary: These topics demonstrate how difficult it is to prove a significant change in outcome in high-risk CAD patients by prophylactic preoperative measures and that there is no alternative to clinical judgment and individualized patient care.

Rationale: The cytosolic protease calpain has been recently implicated in the vascular remodeling of angiotensin II (Ang II) type 1 receptor (AT(1)R) signaling. The role of Ang II/AT(1)R/calpain signaling on endothelial function, an important and early determinant of vascular pathology, remains though totally unknown. Accordingly, we investigated the role of calpain in the endothelial dysfunction of Ang II., Objective: To demonstrate a mechanistic role for calpain in the endothelial dysfunction induced by Ang II/AT(1)R signaling. To establish endothelial-expressed calpains as an important target of AT(1)R signaling., Methods and Results: Subchronic administration of nonpressor doses of Ang II to rats and mice significantly increased vascular calpain activity via AT(1)R signaling. Intravital microscopy studies revealed that activation of vascular expressed calpains causes endothelial dysfunction with increased leukocyte-endothelium interactions and albumin permeability in the microcirculation. Western blot and immunohistochemistry studies confirmed that Ang II/AT(1)R signaling preferentially activates the constitutively expressed μ-calpain isoform and demonstrated a calpain-dependent degradation of IκBα, along with upregulation of nuclear factor κB-regulated endothelial cell adhesion molecules. These physiological and biochemical parameters were nearly normalized following inhibition of AT(1)R or calpain in vivo. RNA silencing studies in microvascular endothelial cells, along with knockout and transgenic mouse studies, further confirmed the role of μ-calpain in the endothelial adhesiveness induced by Ang II., Conclusions: This study uncovers a novel role for calpain in the endothelial dysfunction of Ang II/AT(1)R signaling and establishes the calpain system as a novel molecular target of the vascular protective action of renin-angiotensin system inhibition. Our results may have significant clinical implications in vascular disease.

Background: In a previous study it has been shown that a long-term survival score (LTSS), composed of Lee's Revised Cardiac Risk Index (RCRI) criteria supplemented by age, preoperative electrocardiography (EKG) features, and all types of diabetes to the RCRI criteria, predicts long-term (3-15 years) survival after major vascular surgery. The present study aimed to investigate the performance of LTSS in predicting earlier survival (3 months-3 years) as compared with the RCRI., Methods: Data from 921 consecutive patients undergoing major vascular surgery (624 patients at Hadassah Medical Center [HMC] and 296 patients in Beth Israel Deaconess Medical Center [BIDMC]) were collected retrospectively. The LTSS was seven points that included the five RCRI factors as well as age >65 years and ST-segment depression on preoperative EKG. Logistic regression and receiver operating characteristic curve (ROC) curve analyses were used to compare the 3 months-3 years mortality between the RCRI and LTSS., Results: The Beth Israel Deaconess Medical Center patients were sicker than the Hadassah Medical Center patients, with higher RCRI (1.2 ± 1.0 vs. 0.81 ± 0.83, p < 0.001) and LTSS (2.6 ± 1.4 vs. 1.7 ± 1.2, p < 0.001) and higher 3-years mortality (36.3% vs. 20.7%, p = 0.005). The LTSS predicted mortality better than RCRI as measured by the area under the ROC curves at all time points between 6 months (0.66 ± 0.03 vs. 0.57 ± 0.04, p = 0.02) and 3 years (0.70 ± 0.02 vs. 0.61 ± 0.02, p < 0.0001) in both institutions, but not 3-months mortality. The LTSS also provided better discrimination between each adjacent two-risk score than the RCRI., Conclusions: Age >65 years, ST-segment depression on preoperative 12-lead EKG, and all types of diabetes added to the RCRI significantly improved the preoperative prediction of mortality after 6 months following major vascular surgery., (Copyright © 2011 Annals of Vascular Surgery Inc. Published by Elsevier Inc. All rights reserved.)

Background: Thoracoabdominal aortic aneurysm repair requires complex surgery. Clamping of the descending aorta during the operation results in organ malperfusion, ischemia, and in some cases, irreversible end-organ damage and death. Several methods for organ preservation during the operation evolved, resulting in decreased post-operative organ malfunction. Re-attachment of intercostal arteries, cerebrospinal fluid drainage, and temporary bypass of the clamped aorta and selective perfusion of the spinal cord, intestine, liver and kidneys are widely used during the operation., Objectives: To determine the impact of implementation of protective measures on the outcome of thoracoabdominal surgery over a decade., Methods: Between March 1993 and March 2003, 11 patients (age 41-80 years, average 60 years) underwent thoracoabdominal aortic aneurysm repair in our hospital. Different methods for organ preservation were used during the operation., Results: The early survival is 91%. One patient suffered from paraplegia and one from mild temporary paraparesis. Two patients died during the follow-up period (at 5 months from pneumonia and at 2 years from aortic arch rupture)., Conclusions: Implementation of all adjuncts to protect the organs dependent on aortic perfusion may eliminate the ischemic consequences of aortic clamping.

Aims: Guidelines advocate selective non-invasive testing before major non-cardiac surgery, yet data defining who may benefit from such tests is lacking. We aimed to find the predictors that define patients who are most likely to benefit from preoperative cardiac testing and coronary revascularization (CR)., Methods and Results: In 624 consecutive major vascular surgery patients, the preoperative thallium scanning (PTS) results and subsequent CRs were correlated with long-term (3-15 years) survival. Of all patients, 510 (80.6%) had PTS, 154 (24.7%) had moderate-severe ischaemia on PTS, and 96 (15.4%) underwent CR. Seven predictors: age >or=65, diabetes, cerebrovascular disease, ischaemic heart disease, congestive heart failure, ST-depression on preoperative ECG, and renal insufficiency, independently determined long-term survival. A long-term survival score (LTSS) comprised of these predictors, divided all patients into low, intermediate, and high-risk groups (0-1, 2-3, >or=4 predictors, respectively) with a 5-year survival of 83 +/- 2%, 60 +/- 3%, and 34 +/- 6%, respectively. Compared with low-risk patients, intermediate and high-risk patients had worse survival [HR (CI) = 2.6 (2.0-3.4) and 5.9 (4.1-8.9), respectively, P < 0.001]. Yet, only the intermediate-risk group had better long-term survival following preoperative CR [HR = 0.48 (0.31-0.75), P = 0.001]. The low-risk groups' favourable survival and high-risk groups' poor survival were not significantly affected by CR., Conclusion: Intermediate-risk patients (LTSS 2-3) are most likely to have a long-term survival benefit from PTS and CR.

Purpose of Review: With the graying of the Western population, there is a continuous increase in the proportion of elderly patients undergoing surgical procedures. Geriatric anesthesia is emerging from a 'subspecialty' to the mainstream of today's anesthesia and perioperative care. Much has been written on anesthesia for the elderly, but this review will concentrate on selected topics related to elderly care that represent current unresolved and pertinent issues for the care of the elderly surgical patient., Recent Findings: Postoperative cognitive dysfunction, cardiac diastolic dysfunction and prophylactic perioperative beta-blockade in the process of major noncardiac surgery are three main topics that have recently attracted great interest in clinical practice and research, and have therefore been chosen as the selected topics for this current review., Summary: Although age is a clear risk factor for postoperative cognitive dysfunction, the association of general anesthesia with cognitive dysfunction is less clear, as is the effect of anesthesia per se or surgery on long-term cognitive dysfunction. Cardiac diastolic dysfunction is a relatively new and evolving concept in anesthesia and perioperative medicine, yet clearly diastolic dysfunction even with a normal ejection fraction may have a significant effect on the perioperative outcome and management of elderly patients. Small, but powerful studies have shown significant outcome benefit with prophylactic perioperative beta-blockade in high-risk patients undergoing major noncardiac surgery. Data from other studies, however, are still conflicting and the final verdict awaits larger scale outcome studies.

Introduction: Guideline-directed therapy during the first minutes of resuscitation may be life saving. This study assessed the performance of American Heart Association (AHA) guidelines by trained departmental staff in the period between discovery of collapse and emergency team arrival., Methods: Over a period of 24 months, departmental performance prior to the arrival of the emergency team (median 180 s) was assessed by debriefings conducted within 24h of each event in a 740-bed tertiary hospital with a dedicated certified resuscitation team. Outcome measures were failure to meet AHA treatment recommendations (primary) and return of spontaneous circulation (ROSC)/survival to hospital discharge (secondary)., Results: Two hundred and forty four events were included (216 patients). Mean age was 69+/-17 years; 45% were women. The underlying causes of collapse were mainly cardiac (39%) or respiratory (32%). Residents conducted most of the resuscitations (69%) prior to the arrival of the emergency team. Basic diagnostic measures such as assessments of pulse and rhythm were not performed in 19 and 33% of events. Therapeutic measures such as positive pressure ventilation, chest compressions and defibrillation were not provided according to the guidelines in 17, 12 and 44% of the events. ROSC occurred in 62% of events; 54% of VF/VT, 30% of asystole, 22% of PEA and 76% of bradyarrhythmias/severe bradycardias. Survival to hospital discharge was 37% overall and 41% for patients found in VF/VT (n=33)., Conclusions: Trained departmental staff performed poorly in the moments between patient discovery and arrival of the emergency team. Since patient outcomes were comparable to those described in the literature, poor resuscitation performance may be commonplace in hospitals where ward personnel are expected to deliver advanced life support prior to arrival of the emergency team.

Objectives: We sought to determine the role of preoperative predictors, particularly ischemia, on preoperative thallium scanning (PTS) and coronary revascularization on low-level and conventional troponin elevations after major vascular surgery., Background: Postoperative cardiac troponin (cTn) elevations have recently been shown to predict both short- and long-term mortality after vascular surgery., Methods: The perioperative data, including PTS and subsequent coronary revascularization, continuous perioperative 12-lead ST-segment trend monitoring, cTn-I and/or cTn-T, and creatine kinase-MB fraction in the first three postoperative days, were prospectively collected in 501 consecutive elective major vascular procedures., Results: Moderate to severe inducible ischemia on PTS was associated with a 49.0% incidence of low-level (cTn-I >0.6 and/or cTn-T >0.03 ng/ml) and 22.4% conventional (cTn-I >1.5 and/or cTn-T >0.1 ng/ml) troponin elevation. In contrast, patients with preoperative coronary revascularization had 23.4% and 6.4% low-level and conventional troponin elevations, respectively, similar to patients without ischemia on PTS. By multivariate logistic regression, ischemia on PTS was the most important predictor of both low-level and conventional troponin elevations (adjusted odds ratios [ORs] 2.5 and 2.7, p = 0.02 and 0.04, respectively), whereas preoperative coronary revascularization predicted less troponin elevations (adjusted ORs 0.35 and 0.16, p = 0.045 and 0.022, respectively). Postoperative ischemia (>10 min), the more so prolonged (>30 min) ischemia was the only independent predictor of troponin elevation if added with the preoperative predictors to the multivariate analysis (ORs 15.8 and 22.8, respectively, p < 0.001)., Conclusions: Troponin elevations occur frequently after vascular surgery. They are strongly associated with postoperative ischemia, predicted by inducible ischemia on PTS, and reduced by preoperative coronary revascularization.

A novel physiological cardiac assist device (PCAD), otherwise known as the LEVRAM assist device, which is synchronized with the heartbeat, was developed to assist the left ventricle (LV) in chronic heart failure (CHF). The PCAD utilizes a single cannula, which is inserted in less than 15 s through the apex of the beating LV by means of a specially designed device. Blood is withdrawn from the LV into the PCAD in diastole and is injected back to the LV, through the same cannula, during the systolic ejection phase, thereby augmenting stroke volume (SV) and stroke work (SW). CHF with dilated LV was induced in sheep by successive intracoronary injections of 100-microm beads. The sheep (92.2 +/- 25.9 kg, n = 5) developed stable CHF with increased LV end-diastolic diameter (69.4 +/- 3.3 mm) and end-diastolic volume (LVEDV = 239 +/- 32 mL), with severely reduced ejection fraction (23.8 +/- 7.6%), as well as mild-to-moderate mitral regurgitation. The sheep were anesthetized, and the heart was exposed by left thoracotomy. Pressure was measured in the LV and aorta (Millar). The SV was measured by flow meters and the LV volume by sonocrystals. Assist was provided every 10 regular beats, and the assisted beats were compared with the preceding unassisted beats, at the same LVEDV. The PCAD displaced 13.6 +/- 3.4 mL, less than 8% of LVEDV. Added SW was calculated from the assisted and control pressure-volume loops. The efficiency, defined as an increase in SW divided by the mechanical work of the PCAD, was 85.4 +/- 16.9%. We conclude that the PCAD, working with a small displaced blood volume in synchrony with the heartbeat, efficiently augments the SW of the dilated failing LV. The PCAD is suggested for use as a permanent implantable device in CHF.

Objectives: The aim of this study was to determine the long-term prognosis with postoperative markers of myocardial ischemia and infarction., Background: Cardiac troponins (cTn) are superior to creatine kinase-MB fraction (CK-MB) in detecting perioperative myocardial infarction (PMI). However, their threshold levels signifying PMI and their long-term prognostic value are not yet determined., Methods: A cohort of 447 consecutive patients who underwent 501 major vascular procedures was prospectively studied. Perioperative continuous 12-lead electrocardiogram monitoring, cardiac troponin-I (cTn-I) and/or cardiac troponin-T (cTn-T), and CK-MB levels on the first three postoperative days, and long-term survival were determined. The association of different cutoff levels of CK-MB, troponin, and ischemia duration with long-term survival was investigated., Results: Between 14 (2.9%) and 107 (23.9%) of the patients sustained PMI, depending on the biochemical criteria used. Elevated postoperative CK-MB, cTn, and prolonged (>30 min) ischemia, at all cutoff levels examined, predicted long-term mortality independent of the preoperative predictors: patient's age, type of vascular surgery, previous myocardial infarction, and renal failure (Cox multivariate analysis). Both CK-MB >10% and cTn-I >1.5 ng/ml and/or cTn-T >0.1 ng/ml independently predicted a 3.75-fold and 2.06-fold increase in long-term mortality (p = 0.006 and 0.012, respectively). Similarly, both CK-MB >5% and cTn-I >0.6 ng/ml and/or cTn-T >0.03 ng/ml independently predicted a 2.15-fold and 1.89-fold increase in mortality (p = 0.018 and 0.01, respectively). Patients with both these markers elevated had a 4.19-fold increase in mortality (p < 0.001)., Conclusions: Postoperative CK-MB and troponin, even at low cutoff levels, are independent and complementary predictors of long-term mortality after major vascular surgery.

We developed the Guideline Execution by Semantic Decomposition of Representation (GESDOR) model to share guidelines encoded in different formats at the execution level. For this purpose, we extracted a set of generalized guideline execution tasks from the existing guideline representation models. We then created the mappings between specific guideline representation models and the set of the common guideline execution tasks. Finally, we developed a generic task-scheduling model to harmonize the existing approaches to guideline task scheduling. The evaluation has shown that the GESDOR model can be used for the effective execution of guidelines encoded in different formats, and thus realizes guideline sharing at the execution level.

Background: Perioperative myocardial ischemia is conventionally monitored using five electrocardiographic leads, with only one precordial lead placed at V5. This is based on studies from more than a decade ago. The authors reassessed this convention by analyzing data obtained from continuous on-line 12-lead electrocardiographic monitoring., Methods: One hundred eighty-five consecutive patients undergoing vascular surgery were monitored by continuous 12-lead ST-trend analysis during and for 48-72 h after surgery. Cardiac troponin I was measured in the first 3 postoperative days, and cardiac outcome was prospectively recorded. Ischemia was defined as ST deviation, relative to the reference preanesthesia electrocardiogram, of 0.2 mV or more in one lead or 0.1 mV or more in two contiguous leads, lasting more than 10 min., Results: During 11,132 patient-hours of monitoring, 38 patients (20.5%) had 66 transient ischemic events, with all but one denoted by ST-segment depression. Twelve patients (6.5%) sustained postoperative infarction (cardiac troponin I > 3.1 ng/ml). Among the 38 patients with ischemia, lead V3 most frequently (86.8%) demonstrated ischemia, followed by V4 (78.9%) and V5 (65.8%). Among the 12 patients with infarction, V4 was most sensitive to ischemia (83.3%), followed by V3 and V5 (75% each). Combining two precordial leads increased the sensitivity for detecting ischemia (97.4% for V3 + V5 and 92.1% for either V4 + V5 or V3 + V4) and infarction (100% for V4 + V5 or V3 + V5 and 83.3% for V3 + V4). On average, baseline preanesthesia ST was above isoelectric in V1 through V3 and below isoelectric in V5 through V6. Lead V4 was closest to the isoelectric level on the baseline electrocardiogram, rendering it most suitable for ischemia monitoring., Conclusions: As a single lead, V4 is more sensitive and appropriate than V5 for detecting prolonged postoperative ischemia and infarction. Two precordial leads or more are necessary so as to approach a sensitivity of greater than 95% for detection of perioperative ischemia and infarction.

Objectives: The goal of this study was to investigate the nature of the association between silent ischemia and postoperative myocardial infarction (PMI)., Background: Silent ischemia predicts cardiac morbidity and mortality in both ambulatory and postoperative patients. Whether silent stress-induced ischemia is merely a marker of extensive coronary artery disease or has a closer association with infarction has not been determined., Methods: In 185 consecutive patients undergoing vascular surgery, we correlated ischemia duration, as detected on a continuous 12-lead ST-trend monitoring during the period 48 h to 72 h after surgery, with cardiac troponin-I (cTn-I) measured in the first three postoperative days and with postoperative cardiac outcome. Postoperative myocardial infarction was defined as cTn-I >3.1 ng/ml accompanied by either typical symptoms or new ischemic electrocardiogram (ECG) findings., Results: During 11,132 patient-hours of monitoring, 38 patients (20.5%) had 66 transient ischemic events, all but one denoted by ST-segment depression. Twelve patients (6.5%) sustained PMI; one of those patients died. All infarctions were non-Q-wave and were detected by a rise in cTn-I during or immediately after prolonged, ST depression-type ischemia. The average duration ofischemia in patients with PMI was 226+/-164 min (range: 29 to 625), compared with 38+/-26 min (p = 0.0000) in 26 patients with ischemia but not infarction. Peak cTn-I strongly correlated with the longest, as well as cumulative, ischemia duration (r = 0.83 and r = 0.78, respectively). Ischemic ECG changes were completely reversible in all but one patient who had persistent new T wave inversion. All ischemic events culminating in PMI were preceded by an increase in heart rate (delta heart rate = 32+/-15 beats/min), and most (67%) of them began at the end of surgery and emergence from anesthesia., Conclusions: Prolonged, ST depression-type ischemia progresses to MI and is strongly associated with the majority of cardiac complications after vascular surgery.

Step baroreceptor stimulation can provide an insight into the baroreflex control mechanism, yet this has never been done in humans. During carotid surgery under regional anesthesia, a step increase in baroreceptor stimulation occurs at carotid declamping immediately after removal of the intra-arterial atheromatous plaque. In 10 patients, the R-R interval and systolic and diastolic blood pressures (BP) were continuously recorded, and signals obtained within the time window from 10 min before until 10 min after carotid declamping were analyzed. Mean +/- SD time signals, power spectra, and transfer and coherence functions before and after declamping were calculated. Immediately after carotid declamping, both heart rate (HR) and BP declined in an exponential-like manner lasting 10.3 +/- 5.9 min, and their power spectra increased in the entire frequency range. Transfer function magnitude and coherence functions between BP and HR increased predominantly in the midfrequency region (approximately 0.1 Hz), with no change in phase function. Thus, in carotid endarterectomy patients, step increase in baroreceptor gain elicits a prolonged decline in HR and BP. Frequency analyses support the notion that the baroreflex control mechanism generates the midfrequency HR and BP variability, although other frequency regions are also affected.

Purpose: To investigate the associations between specific preoperative 12-lead electrocardiogram (ECG) abnormalities, perioperative ischemia, and postoperative myocardial infarction or cardiac death in major vascular surgery., Methods: Two prospective studies on perioperative myocardial ischemia performed in two tertiary university hospitals were combined to include 405 patients. All preoperative ECGs were analyzed according to the Sokolow-Lyon criteria for left ventricular hypertrophy by investigators who were blinded to the patients' perioperative clinical course. Perioperative myocardial ischemia was detected by continuous ECG recording, and postoperative cardiac complications included myocardial infarction and cardiac death., Results: A total of 19 postoperative cardiac complications occurred (two cardiac deaths and 17 myocardial infarctions). Voltage criteria for left ventricular hypertrophy (78 patients, 19%) and ST segment depression greater than 0.5 mm (98 patients, 24.2%) on preoperative ECGs were both significantly associated with postoperative myocardial infarction or cardiac death (odds ratio, 4.2 and 4.7; p = 0.001 and 0.0005, respectively) and with longer intraoperative and postoperative myocardial ischemia. In each of the two study groups, a preoperative ECG abnormality that involved voltage criteria, ST segment depression, or both (134 patients, 33.1%) was more predictive of postoperative cardiac complications than any other preoperative clinical variable, including a history of myocardial infarction or angina pectoris, diabetes mellitus, pathologic Q-wave by ECG, or preoperative myocardial ischemia. The combined duration of intraoperative and postoperative ischemia and the preoperative ECG with either voltage criteria or ST segment depression were the only independent factors associated with adverse cardiac events by multivariate analysis (p < or = 0.0001 and p = 0.02, respectively)., Conclusion: Left ventricular hypertrophy and ST segment depression on preoperative 12-lead ECGs are important markers of increased risk for myocardial infarction or cardiac death after major vascular surgery.

The importance of prolonged postoperative myocardial ischaemia in cardiac outcome has recently been emphasised. The present study examines the correlation between perioperative ischaemia and myocardial infarction (MI) in patients undergoing peripheral vascular surgery (PVS) under regional anaesthesia. One-hundred-and-forty consecutive peripheral vascular operations under regional anaesthesia were prospectively analysed, using Holter monitoring for perioperative myocardial ischaemia (defined as down sloping or horizontal ST-segment depression of > or = 1 mm) and postoperative cardiac outcome. The study was approved after informed consent. There were 82 carotid endarterectomies under cervical block and 58 infrainguinal bypass procedures under continuous spinal or epidural anaesthesia. IHD was present in 53.6% cases: previous MI-38%; angina pectoris-33%; previous CABG/PTCA-24%. Holter monitoring started about 20 hours before surgery and continued for 45 hours. After surgery patients were followed for signs of cardiac complications; daily 12 lead ECG; 6 hourly CK-MB isoenzymes during the first 24 postoperative hours and later whenever indicated. MI diagnosis was based on chest pain, permanent new ECG changes and CK-MB elevation. There was no 30-day mortality. Postoperative MI occurred in seven patients (5%). Five of the postoperative MI were non-Q-wave infarctions. The majority (71%) of the adverse cardiac events started within 24 hours of surgery, and the latest occurred 52 and 72 hours post surgery. In 65 cases (46.4%) there were 259 episodes of significant ST-depression. In 75 (53.6%) cases ischaemic episodes were not detected. Patients with postoperative cardiac events had significantly more and longer ischaemic episodes in all three perioperative periods than those without such events.(ABSTRACT TRUNCATED AT 250 WORDS)

Perioperative myocardial ischemia was evaluated in 36 consecutive carotid endarterectomy procedures carried out on patients with a high (72.2%) prevalence of ischemic heart disease. The procedures were performed under cervical plexus block plus a prophylactic intravenous nitroglycerin infusion. Findings of myocardial ischemia on perioperative (48 hours) continuous electrocardiogram recordings were correlated with preoperative cardiac status, perioperative continuous intra-arterial blood pressure measurements, and postoperative cardiac outcome. In two patients, ST segment analysis was un-interpretable because of bundle-branch blocks. Altogether, 64 episodes of significant ST segment depression were detected in 18 (52.9%) of the remaining procedures. In 8 (23.5%) procedures, ST segment depressions occurred either during carotid artery clamping at the time of the largest rise in blood pressure or within 2 hours of declamping, when blood pressure tended to decline. There were four (11.7%) postoperative cardiac events: three myocardial infarctions (one Q wave and two non-Q wave) and one episode of unstable angina pectoris. All four patients with cardiac events had early signs of myocardial ischemia either at the time of cross-clamping, or soon after declamping of the carotid artery. All myocardial infarctions developed following prolonged (> 10 hours) myocardial ischemia, starting with the first 20 hours after surgery. Thus, ST segment depression occurring during clamping or soon after carotid declamping was associated with cardiac complications (sensitivity 100% and specificity 86.6%) and suggests the possible usefulness of on-line ST segment trend monitoring.

Multiresolution representations of the heart rate variability (HRV) using the wavelet transforms are proposed to characterize the autonomic nervous system regulation of cardio-vascular activity during carotid surgery. Results suggest that the power in all frequency bands was low during the surgery and increased after the declamping of the carotid artery.

Acute, massive pulmonary embolism is life-threatening and must be treated immediately. Since the early 1970's when thrombolytic therapy was shown to hasten resolution of pulmonary emboli, there has been a debate in the literature as to new indications for surgical pulmonary embolectomy. Some authors believed that there are no longer any indications for embolectomy, while others justify surgery for certain indications. Although the debate is still on, this operation is very rarely performed today. We present a patient who developed massive pulmonary embolism, with continuing extreme hemodynamic and respiratory disturbances despite full thrombolytic treatment. Embolectomy was successfully performed.

Intrapleural marcaine has been described as an effective method of analgesia following upper abdominal and thoracic operations and is no longer regarded as experimental. We have shown that the same quality of analgesia can be achieved by injecting the drug through a catheter inserted intraoperatively through the surgical incision. In our method, applied in 9 cases, there is no risk of pneumothorax as a result of piercing the chest wall, since intraoperative placement of the intrapleural catheter is very easy. We therefore suggest it as the method of choice for postoperative analgesia in kidney operations. It is especially recommended in elderly patients with chronic pulmonary disease who do not tolerate narcotics well.