Electrocardiographic abnormalities and NT-proBNP levels at long-term follow-up of patients with dyspnea after pulmonary embolism.

OBJECTIVES: Electrocardiogram (ECG) and measurement of plasma brain natriuretic peptides (BNP) are established markers of right ventricular dysfunction (RVD) in the setting of acute pulmonary embolism (PE) but their value at long-term follow-up is largely unknown. The purpose of this prospective study was to determine the prevalence of ECG abnormalities, describe levels of N-terminal proBNP (NT-proBNP), and establish their association with dyspnea at long-term follow-up after PE. DESIGN: All Swedish patients diagnosed with acute PE in 2005 (n = 5793) were identified through the Swedish National Patient Registry. Surviving patients in 2007 (n = 3510) were invited to participate. Of these, 2105 subjects responded to a questionnaire about dyspnea and comorbidities. Subjects with dyspnea or risk factors for development of chronic thromboembolic pulmonary hypertension were included in the study in a secondary step, which involved collection of blood samples and ECG registration. RESULTS: Altogether 49.3% had a completely normal ECG. The remaining participants had a variety of abnormalities, 7.2% had atrial fibrillation/flutter (AF). ECG with any sign of RVD was found in 7.2% of subjects. Right bundle branch block was the most common RVD sign with a prevalence of 6.4%. An abnormal ECG was associated with dyspnea. AF was associated with dyspnea, whereas ECG signs of RVD were not. 61.2% of subjects had NT-proBNP levels above clinical cut-off (>125 ng/L). The degree of dyspnea did not associate independently with NT-proBNP levels. CONCLUSIONS: We conclude that the value of ECG and NT-proBNP in long term follow-up after PE lies mostly in differential diagnostics.

New or presumably new left bundle branch block in patients with suspected acute coronary syndrome: Clinical, echocardiographic, and electrocardiographic features from a single-center registry.

BACKGROUND: In patients with suspected acute coronary syndrome, a new or presumably new left bundle branch block (LBBB) does not always imply ST-segment elevation myocardial infarction (STEMI). We aimed to show the low frequency of STEMI-equivalent in this population and determine the diagnostic value of electrocardiographic and echocardiographic features. METHODS: From the 387 patients captured by the Louisiana State University code STEMI registry between 2009 and 2012, we examined data on 26 patients with LBBB. These patients were divided into 3 groups according to the final diagnosis: (1) STEMI-equivalent, defined as an acute coronary occlusion on angiography (2 patients), (2) non-ST-segment elevation myocardial infarction (4 patients), and (3) diagnoses other than myocardial infarction (non-MI) (20 patients). RESULTS: Troponin elevation and left ventricular systolic dysfunction were common in all 3 groups (non-significant p-values). Compared with non-MI patients, patients with STEMI-equivalent had a larger degree of ST-segment discordance and T-wave discordance, as assessed by ST/QRS and T/QRS ratios (p<0.001). ST/QRS ratio ≥ 0.2 and T/QRS ratio ≥ 0.5 were sensitive and specific for the diagnosis of STEMI-equivalent in the setting of LBBB. Conversely, absolute values of ST-segment and T-wave discordance were not significantly different between groups. ST-segment concordance was highly specific for the diagnosis of STEMI-equivalent, but had a limited sensitivity. CONCLUSION: Only a minority of patients with suspected acute coronary syndrome and LBBB have a STEMI-equivalent. Excessive relative discordance of the ST segment or the T wave appears predictive of STEMI-equivalent, but this is only hypothesis-generating considering the small population size.

A clinical and laboratory approach used to elucidate discordant results of high-sensitivity troponin T and troponin I.

BACKGROUND: Careful interpretation of discordant results in high-sensitivity troponin measurements is necessary in cases of suspect immunoassay interferences. We describe several procedures taken in a case of a polymorbid patient with chest pain, without clear evidence of myocardial necrosis and with increased high-sensitivity cardiac troponin T (hs-cTnT). We checked the Vafaie's algorithm for the evaluation of suspect interference in troponin measurements. METHODS: We conducted a case report analysis, additional measurements, a dilution test and pretreatment of plasma with blocking agents. RESULTS: Concentration of hs-cTnT (99 th percentile of "healthy" population 14 ng/L) increased from 120.1 ng/L to 280.4 ng/L during an 8-month period and decreased to 216.3 ng/L during the following month with repeatedly negative troponin I (TnI), hs-cTnI, myoglobin and creatine kinase MB (CK-MB). Suspected false positivity of hs-cTnT was further confirmed by treatment of plasma with an antiheterophile blocking agent (hs-cTnT before treatment 280.4 ng/L, after 16.53/16.23 ng/L). This outcome was further confirmed by the manufacturer's experiments. CONCLUSIONS: The false-positive results of hs-cTnT were caused by the presence of extremely rare high molecular weight protein, presumably IgM, most likely HAMA (human anti-mouse antibody). Only the pre-treatment of plasma with a blocking agent provided a reliable indication of the interference. Cooperation among clinicians, laboratory personnel and the manufacturer is essential.

Electrophysiological and haemodynamic effects of vernakalant and flecainide in dyssynchronous canine hearts.

AIMS: About one-third of patients with mild dyssynchronous heart failure suffer from atrial fibrillation (AF). Drugs that convert AF to sinus rhythm may further slowdown ventricular conduction. We aimed to investigate the electrophysiological and haemodynamic effects of vernakalant and flecainide in a canine model of chronic left bundle branch block (LBBB). METHODS AND RESULTS: Left bundle branch block was induced in 12 canines. Four months later, vernakalant or flecainide was administered using a regime, designed to achieve clinically used plasma concentrations of the drugs, n = 6 for each drug. Epicardial electrical contact mapping showed that both drugs uniformly prolonged myocardial conduction time. Vernakalant increased QRS width significantly less than flecainide (17 ± 13 vs. 34 ± 15%, respectively). Nevertheless, both drugs equally decreased LVdP/dtmax by ∼15%, LVdP/dtmin by ∼10%, and left ventricular systolic blood pressure by ∼5% (P = n.s. between drugs). CONCLUSIONS: Vernakalant prolongs ventricular conduction less than flecainide, but both drugs had a similar, moderate negative effect on ventricular contractility and relaxation. Part of these reductions seems to be related to the increase in dyssynchrony.

Sodium channel blockade with QRS widening after an escitalopram overdose.

INTRODUCTION: Escitalopram is rarely associated with prolongation of the QTc interval; however, there are no reported cases of QRS complex widening associated with escitalopram overdose. We report a case of a patient who presented with both QRS complex widening and QTc interval prolongation after an escitalopram overdose. CASE: A 16-year-old girl presented to the emergency department after ingestion of escitalopram, tramadol/acetaminophen, and hydrocodone/acetaminophen. Laboratory results were significant for 4-hour acetaminophen 21.1 µg/mL. Serum electrolytes including potassium, magnesium, and calcium were all normal. Initial electrocardiogram (ECG) revealed a widened QRS with an incomplete right bundle branch pattern. After administration of 100-mEq sodium bicarbonate, a repeat ECG revealed narrowing of the QRS complex and a prolonged QTc interval. Magnesium sulfate 2 g intravenous and sodium bicarbonate drip were initiated. A repeat ECG, 1 hour after the second, revealed normalization of the QRS complex and QTc interval. DISCUSSION: Prolongation of the QTc interval is an expected effect of escitalopram. Both escitalopram and citalopram are metabolized to the cardiotoxic metabolite S-didesmethylcitalopram and didesmethylcitalopram, respectively, which have been implicated in numerous cardiac abnormalities including widening of the QRS complex. Although never previously described with escitalopram, this mechanism provides a reasonable explanation for the QRS complex widening and incomplete right bundle branch block that occurred in our patient. CONCLUSIONS: Both QRS complex widening and QTc interval prolongation should be monitored in cases of escitalopram and citalopram overdoses.

Usefulness of QRS axis change to predict mortality in patients with left bundle branch block.

QRS duration correlates with poor prognosis in patients with left bundle branch block (LBBB), but the importance of left-axis deviation (LAD) is not well established. To determine if LAD confers a mortality risk in patients with LBBB, a single-center, retrospective, population-based cohort study was conducted. Included were all patients at 1 hospital with LBBB on electrocardiography from 1995 to 2005 over a 17-year follow-up period (n = 2,794, median follow-up duration 20 months, interquartile range 6 to 64). Half of all patients with LBBB had LAD. The all-cause mortality rate in the entire cohort was 15%. LAD was not associated with mortality, either as a single outcome (odds ratio [OR] 1.1, 95% confidence interval [CI] 0.88 to 1.3, p = 0.50) or in time-to-event analysis (p = 0.40). Significant risk factors for mortality included high creatinine (OR 1.2, 95% CI 1.1 to 1.3), low hemoglobin (OR 1.2, 95% CI 1.1 to 1.3), history of atrial fibrillation (OR 1.6, 95% CI 1.3 to 2.1), electrocardiographic evidence of previous infarct (OR 1.5, 95% CI 1.2 to 1.9), and history of ventricular tachycardia (OR 1.4, 95% CI 1.0 to 1.9). On bivariate analysis, LAD was associated with atrial fibrillation, ventricular tachycardia, age, and congestive heart failure. Patients with LBBB who converted from normal axis to LAD had significantly higher mortality in time-to-event analysis (p = 0.02). In conclusion, in patients with LBBB, LAD does not confer significant mortality risk. However, those with normal axis who developed LAD during the study period had significantly higher mortality. Perhaps when LBBB and LAD develop concurrently, there is no increased risk over baseline LBBB development, but it may herald a worse prognosis if LAD develops against the background of previous LBBB, from an unknown mechanism.

[Early invasive strategy in patients with myocardial infarction and intraventricular conduction disturbances and plasma B-type natriuretic peptide levels assessed 6 months after myocardial infarction]. / Wczesna strategia inwazyjna u chorych z zawalem serca i zaburzeniami przewodzenia sródkomorowego a stezenie peptydu natriuretycznego typu B w surowicy oceniany 6 miesiecy po zawale serca.

UNLABELLED: The aim of the study was to assess plasma B-type natriuretic peptide (BNP) levels in patients after myocardial infarction (MI) with intraventricular conduction defects (IVCD) and to define relationship between BNP level, treatment strategy and left ventricular performance. MATERIAL AND METHODS: Four types of IVCD were noted: left bundle branch block (LBBB), right bundle branch block (RBBB), left anterior hemiblock (LAH) and left posterior hemiblock (LPH). A total of 158 patients six months after MI treated either invasively or conservatively were included. Of them 126 had IVCD (group A): LBBB-31, RBBB-36, LAH-130, LPH-29, whereas 32 patients without IVCD served as controls (group B). Plasma BNP levels were measured using an immunoenzymatic method. All subjects underwent echocardiography to evaluate left ventricular function. RESULTS: In group A significantly lower plasma BNP levels (186.3 vs 355.3 pg/mL; p < 0.01) and significantly higher left ventricular ejection fraction (EF) (48.4 vs 42.4%; p < 0.05) were noted in favour of invasive treatment. In group B differences between plasma BNP level and echocardiographic parameters of left ventricle function were insignificant. In patients with LBBB plasma BNP levels were significantly lower in those treated invasively (163.9 vs 528.9; p < 0.01). Also, left ventricular EF and myocardial performance index (MPI) were comparable, whereas E/A value was lower as compared with patients treated conservatively (p < 0.05). There were no significant differences in BNP levels in groups with RBBB, LAH and LPH. Multifactorial regression analysis showed that BNP levels were most strongly correlated with magnitude of the ejection fraction EF (p < 0.001). Other parameters which affect significantly BNP level were MPI: OR 9.07 (95% CI 1.03-79.58; p < 0.05) and E/A: OR 6.58 (95% CI 1.01-42.76; p < 0.05). CONCLUSIONS: Invasive strategy in MI with IVCD, especially with LBBB, correlates with lower plasma BNP levels six months after index procedure. In patients with IVCD post MI plasma BNP level is better marker of dysfunction of the left ventricle than its ejection fraction.

Post-myocardial infarction intraventricular conduction defects and B-type natriuretic peptide levels.

BACKGROUND: Levels of B-type natriuretic peptide (BNP), a significant marker of left ventricular (LV) dysfunction, may provide information on the severity of heart failure in patients with intraventricular conduction defects (IVCD).The aim of this study was to measure serum BNP levels in post-myocardial infarction (MI) patients with IVCD. METHODS: In 2004-2005 during standard follow-up at 6 mo after acute MI in 158 subjects, BNP was measured using an immunoenzymatic method. Of them, 126 patients had IVCD: 31, left bundle branch block (LBBB); 36, right bundle branch block (RBBB); 30, left anterior hemiblock (LAH); and 29, left posterior hemiblock (LPH). Thirty two patients with a previous MI, but without IVCD, served as controls, whereas 15 healthy subjects entered the comparative group. RESULTS: In post-MI patients with IVCD, the mean BNP level was significantly higher than in their counterparts without IVCD (p < 0.001) and in healthy subjects (p < 0.001). The highest BNP level was found in patients with LBBB and RBBB. In patients with LAH and LPH, levels of BNP were insignificantly higher than in patients without IVCD. CONCLUSIONS: Significantly higher BNP levels in patients with previous MI and IVCD suggest more severe heart failure than in their counterparts without IVCD with comparable LV ejection fraction.

Changing axis deviation and elevation of prostate-specific antigen during acute myocardial infarction.

Left bundle branch block with changing axis deviation also during acute myocardial infarction has been rarely reported. Changing axis deviation with changing bundle branch block during acute myocardial infarction has also been rarely reported. Prostate-specific antigen (PSA) is an established tool in detecting prostate cancer. Immediately after 15 min of exercise on a bicycle ergometer, serum PSA concentrations increased by as much as threefold. Apparently spurious result has been reported in a work about mean serum PSA concentration during acute myocardial infarction with mean serum PSA concentration significantly lower on day 2 than either day 1 or day 3 and it has been reported that these preliminary results could reflect several factors, such as antiinfarctual treatment, reduced physical activity or an acute-phase response. We present a case of changing axis deviation and elevation of serum PSA concentration in a 92-year-old Italian man with acute myocardial infarction. Our report confirms previous findings and extends the evaluation of PSA during acute myocardial infarction.

Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism.

The assessment of risk and appropriate treatment of patients with acute pulmonary embolism (PE) remains a challenge. The prognostic performance of cardiac troponin I (cTnI) in predicting 30-day all-cause mortality was prospectively assessed in consecutive haemodynamically stable patients with PE. The present study included 318 haemodynamically stable patients with PE. During the 30-day study period, 23 (7%) patients died. cTnI was elevated (>or=0.1 ng x mL(-1)) in 102 (32%) patients. An age >65 yrs, systolic blood pressure <120 mmHg and severity of illness assessed using the PE severity index (PESI) were significantly associated with an increased risk for mortality, but no significant association was found between elevation of cTnI and 30-day mortality in a logistic regression analysis. When only fatal PE was considered, multivariate analysis showed that severity of illness using the PESI and an elevated cTnI (odds ratio 3.7, 95% confidence interval (CI) 1.1-12.8) were associated with a significant increase in the risk for death. The negative predictive value (95% CI) of a negative cTnI for mortality was 93 (90-97)%. In conclusion, in haemodynamically stable patients with acute pulmonary embolism, cardiac troponin I was not an independent predictor of 30-day all-cause mortality, although it did predict fatal pulmonary embolism.

Left bundle branch block in chronic heart failure-impact on diastolic function, filling pressures, and B-type natriuretic peptide levels.

BACKGROUND: For patients with chronic heart failure (CHF), left bundle branch block (LBBB) is associated with impaired systolic function and increased morbidity and mortality, but data on diastolic function are scarce. In this patient population, we attempted to define the impact of LBBB on diastolic function, filling pressures, and brain natriuretic peptide and its circulating N-terminal precursor (NT-proBNP) levels. METHODS: A total of 94 patients with stable CHF (48 with complete LBBB, 46 without intraventricular conduction delay and normal QRS duration) underwent conventional 2-dimensional/Doppler echocardiography and Doppler tissue analysis of mitral annular velocities. As a measure of left ventricular filling pressures, the ratio of peak early mitral flow velocity to peak early diastolic mitral annular velocity was derived. NT-proBNP measurements were carried out on a bench-top analyzer (Elecsys-2010, Roche Diagnostics, Mannheim, Germany). RESULTS: Patients with or without LBBB did not differ with respect to the cause of CHF or ejection fraction, but in LBBB deceleration time was shorter (163 +/- 66 vs 205 +/- 95 milliseconds, P = .021) and a restrictive mitral filling pattern was more frequent (35% vs 11%, P = .005). In such patients, the ratio of peak early mitral flow velocity to peak early diastolic mitral annular velocity was higher (14.5 +/- 6.2 vs 10.6 +/- 5.2, P < .001) and NT-proBNP was elevated (3553 +/- 3725 vs 850 +/- 896 pg/mL, P < .01) as compared with patients without LBBB. CONCLUSION: For patients with CHF and comparable systolic performance, LBBB is associated with more severe diastolic dysfunction, elevated filling pressures, and higher NT-proBNP levels. These findings may contribute to increased morbidity and mortality of such patients.

Comorbidity and myocardial dysfunction are the main explanations for the higher 1-year mortality in acute myocardial infarction with left bundle-branch block.

BACKGROUND: The purpose of this study was to assess the independent contribution of left bundle-branch block (LBBB) on cause-specific 1-year mortality in a large cohort with acute myocardial infarction (MI). METHODS AND RESULTS: We studied a prospective cohort of 88,026 cases of MI from the Register of Information and Knowledge about Swedish Heart Intensive care Admissions in 72 hospitals in 1995 to 2001. Long-term mortality was calculated by Cox regression analysis, adjusted for multiple covariates that affect mortality by calculation of a propensity score. LBBB was present in 9% (8041 of 88,026) of the MI admissions. Patients with LBBB were older and had a higher prevalence of comorbid conditions than patients with no LBBB. The unadjusted relative risk of death within 1 year was 2.16 (95% CI, 2.08 to 2.24; P<0.001) for LBBB (42%, 3350 of 8041) compared with those with no LBBB (22%, 17,044 of 79,011). After adjustment for a propensity score that takes into account differences in risk factors and acute intervention, LBBB was associated with a relative risk of death of 1.19 (95% CI, 1.14 to 1.24; P<0.001). In a subgroup of 11,812 patients for whom left ventricular ejection fraction was available and could be added to the analysis, the contributing relative risk of LBBB for death was only 1.08 (95% CI, 0.93 to 1.25; P=0.33). The most common cause of death in both groups was ischemic heart disease. CONCLUSIONS: MI patients with LBBB have more comorbid conditions and an increased unadjusted 1-year mortality. When adjusted for age, baseline characteristics, concomitant diseases, and left ventricular ejection fraction, LBBB does not appear to be an important independent predictor of 1-year mortality in MI.

Effects of glucose-induced insulin secretion on ST segment elevation in the Brugada syndrome.

INTRODUCTION: ST segment elevation in patients with Brugada syndrome is known to fluctuate occasionally, influenced by multiple factors. Insulin has been shown to affect QT dispersion in healthy volunteers, as well as result in abnormality of ventricular repolarization in patients with congenital long QT syndrome. METHODS AND RESULTS: To assess a possible role of insulin in ST segment elevation in patients with Brugada syndrome, an oral glucose tolerance test (OGTT) was administered to 20 patients with Brugada syndrome and 20 normal patients without ST-T changes as a control group. Plasma glucose and potassium levels, immunoreactive insulin concentration (IRI), and ST segment elevation and ST-T wave changes on 12-lead ECG during OGTT were analyzed. Augmentation (>1 mm) of ST elevation or morphologic changes in ST-T waves were observed frequently in response to increased IRI during OGTT [15/20 cases (75%)] in patients with Brugada syndrome but in none of the patients in the control group [0/20 cases (0%), P < 0.01]. The changes returned to baseline 180 minutes after the glucose load in 9 of 15 patients. Patients who showed coved-type ST elevation before the glucose load exhibited positive ECG changes more frequently than patients with saddleback-type elevation or transiently normalized ST segment [8/8 cases (100%) vs 7/12 (58%), P < 0.05]. There was no significant difference between the two groups in terms of glucose, IRI, and potassium levels during OGTT. CONCLUSION: The findings suggest that glucose-induced insulin secretion is one of the contributing factors to fluctuation of ST segment elevation in patients with Brugada syndrome.

[The importance of left bundle branch block in the diagnosis of acute myocardial infarction]. / Kaires Hiso pluosto kojytes blokados reiksme diagnozuojant umini miokardo infarkta.

Electrocardiographic (ECG) evidence of cardiac ischemia or infarction is difficult to detect in the presence of left bundle branch block (LBBB). Traditional ECG indicators of ischemia, such as ST- segment elevation, are common in LBBB and may not indicate acute ischemia. Proper evaluation of the initial ECG is crucial in selecting candidates for early thrombolysis, because the earlier reperfusion treatment is administred, the better are the results. Individuals with LBBB are particularly important stratum of patients to identify. This is true not only because they have a high baseline mortality and receive the greatest incremental improvement in survival when given thrombolytic agents but also because it is tendency to undertreat them. The criteria of Sgarbosa are too insensitive to be used as screening (roule out) test to determine which patients with an LBBB do not have an AMI. The Sgarbosa criteria are, however, highly specific and can be used reliably as confirmatory test to rule in AMI in patients with LBBB. ECG alone doesn't support the diagnosis of AMI. Elevated value of biochemical markers of myocardial necrosis in the presence of LBBB confirms the diagnosis. Despite the recently updated joint practical guidelines of American Heart Association (AHA) and American College of Cardiology (ACC) which defines that all patients having symptoms consistent with acute MI and LBBB should be treated like ST-segment elevation, only minority of them receive thrombolytic therapy, particularly the elderly (only 4%). In the absence of definitive diagnosis of AMI doctors withhold from decision to administer thrombolytic treatment because of risk of haemorrhagic complications. There are not perfect diagnostic tools allowing early diagnostic of AMI in patients having LBBB. Currently the best justified strategy is to follow AHA/ACC recommended guidelines to administer thrombolysis to all patients with LBBB presenting with chest pain, particularly if serum biomarkers are elevated.

Circulating N-terminal brain natriuretic peptide precursor and endothelin levels in patients with syndrome X and left bundle branch block with preserved systolic function.

BACKGROUND: Deterioration of left ventricular function during follow-up was reported in some patients with syndrome X and concomitant left bundle branch block. The patients with syndrome X and left bundle branch block has been frequently presented with elevated Endothelin-1 (ET-1) level while brain natriuretic peptide (BNP) (a sensitive marker of left ventricular dysfunction) has not been measured in patients with syndrome X. METHODS: The purpose of the present study was to assess left ventricular diastolic function, levels of N-terminal Brain Natriuretic Peptide (NT-proBNP) precursor and biochemical parameters of endothelial function in patients with syndrome X complicated by left bundle branch block but preserved left ventricular systolic function (group A, n=8). The echocardiographic and neurohormonal measures in these patients were compared to those in patients with syndrome X without left bundle branch block (group B, n=13), and controls (group C, n=15). RESULTS: At rest and after exercise the serum concentration of NT-proBNP was significantly higher in group A than in the controls (at rest: 232+/-96 vs. 133+/-23 fmol/ml, P=0.03; after exercise: 313+/-96 vs. 180+/-33 fmol/ml, P=0.02). The highest concentration of endothelin-1 was also found in group A, being significantly higher than in the controls (6.81 vs. 4.52 pg/ml, P<0.05). Mitral flow abnormalities were detected in left bundle branch block patients. Accordingly, the lowest E/A ratio was in group A and it differed significantly from that in group C (0.85 vs. 1.1, P<0.05). E/A ratio inversely correlated with plasma NT-proBNP concentration in patients with left bundle branch block (r=-0.48, P=0.02). CONCLUSIONS: Elevated NT-proBNP and endothelin-1 plasma concentrations were demonstrated in patients with syndrome X complicated by left bundle branch block even when left ventricular systolic function was still preserved. In this subgroup the magnitude of left ventricular diastolic dysfunction correlated with the increase of BNP level which reflects neurohormonal activation.

Sex-specific triggers for right ventricular outflow tract tachycardia.

BACKGROUND: Right ventricular outflow tract tachycardia (RVOT-VT) is a common arrhythmia in young patients without heart disease. The arrhythmia is characterized by repetitive bursts and premature ventricular contractions with a left bundle branch block, inferior-axis QRS morphology, and symptoms of palpitations. Although more frequent in women, sex-specific triggers for symptomatic RVOT-VT have not been identified. METHODS AND RESULTS: We interviewed 34 women and 13 men referred for ablation of RVOT-VT to determine if predictable but sex-specific exacerbations in symptomatic RVOT-VT exist. After a general query asking if there was predictability to what triggered palpitations, we then specifically queried all patients about symptomatic RVOT-VT initiation with exercise, stress, caffeine, fatigue, and, in women only, periods of recognized hormonal flux. The times identified as states of hormonal flux included premenstrual, gestational, perimenopausal, and coincident with the administration of birth control pills. In response to the completed interview, the most common recorded trigger for RVOT-VT in women was recognized states of hormonal flux with 20 (59%) of 34 women responding positively and 14 (41%) of the 34 indicating that states of hormonal flux were the only recognizable triggers. Men were more likely than women to report that their RVOT-VT was predictably triggered by exercise, stress, or caffeine: 12 (92%) of 13 men versus 14 (41%) of 34 women (P <.01). CONCLUSIONS: Triggers for RVOT-VT initiation are sex specific. Women have RVOT-VT initiation with recognized states of hormonal flux. Men more commonly have RVOT-VT initiated by exercise or stress. These data have important implications related to patient education and counseling in the setting of RVOT-VT and may influence the timing of drug treatment and electrophysiologic evaluation in selected patients.

Concentration of circulating plasma endothelin in patients with angina and normal coronary angiograms.

BACKGROUND: Some patients with angina pectoris and normal coronary arteriograms have reduced coronary flow reserve and abnormal endothelium dependent vasodilator responses. Endothelin-1 (ET-1), a potent vasoconstrictor, is an important modulator of microvascular function and may also have algogenic properties. METHOD: Plasma ET-1 was measured in peripheral venous blood in 40 patients (30 women) (mean (SD) age 56 (8) years) with angina and normal coronary arteriograms and 21 normal controls (17 women) (mean (SD) age 53 (7) years). Patients with systemic hypertension, left ventricular hypertrophy, or coronary spasm were excluded. Plasma ET-1 was measured using radioimmunoassay. RESULTS: Thirty five patients had > or = 1 mm ST segment depression during exercise. Left bundle branch block was present in four patients at rest and in one during exercise. Mean (SD) (range) concentration of ET-1 (pg/ml) was higher in patients than in controls (3.84 (1.25) (1.97-7.42) v 2.88 (0.71) (1.57-4.48) P < 0.0001). In patients with "high" (> control mean (one SD)) ET-1 concentrations (n = 23), the time to onset of chest pain during exercise was significantly shorter (6.21 (3.9) v 9.03 (3.9) min; p = 0.01) than in patients with "low" ET-1 concentrations. Of the five patients with left bundle branch block, four had plasma ET-1 concentration > 4.0 pg/ml. CONCLUSION: Plasma endothelin is raised in patients with angina and normal coronary arteriograms and is consistent with the demonstration of endothelial dysfunction in such patients. The association between "high" plasma ET-1 and an earlier onset of chest pain during exercise suggests that endothelin may also have a role in the genesis of chest pain in patients with normal coronary arteries.

New bundle branch block after coronary artery bypass grafting--evaluation by CK-MB isoenzyme analysis and transoesophageal echocardiography.

Twelve patients with a new complete bundle branch block after coronary artery bypass grafting underwent transoesophageal echocardiography (TEE). The results of TEE were compared with the pre-operative ventriculography, CK-MB isoenzyme time-release curves and clinical course. In eight patients with transient right bundle branch block or bifascicular block, low CK-MB activities and an uncomplicated postoperative course, transoesophageal echocardiography showed no new segmental wall motion abnormalities apart from a paradoxical septal movement in five. A persistent right or left bundle branch block was associated with either elevated isoenzyme activities, transoesophageal echocardiographic evidence of new segmental wall motion disturbance or both in four patients. One patient died because of fatal arrhythmia and one suffered from a prolonged low cardiac output syndrome. A transient bundle branch block is usually a benign electrocardiographic finding. In case of a persistent bundle branch block associated with elevated CK MB isoenzymes, new left ventricular wall motion disturbances indicating a peri-operative myocardial injury are easily detected by transoesophageal echocardiography.