Repolarization abnormalities in patients with idiopathic ventricular tachycardias

STUDY POPULATION: Twenty patients without laboratory evidence of cardiac disease who underwent electrophysiological study because of recurrent ventricular tachyarrhythmias. PATIENTS AND METHODS: The study population was divided into two groups: group A (20 patients [six males and 14 females] mean age 42.2 +/- 13 years), with idiopathic ventricular tachycardia (VT), and group B (30 controls [10 males and 20 females] mean age 43.6 +/- 16 years). Noninvasive multiparametric analysis of the ventricular repolarization phase was performed on the standard 12-lead electrocardiogram by using a digitizer connected with a computerized system. The intervals JT, heart rate-corrected JT (JTc), JT apex (JTa), heart rate-corrected JTa (JTac), T apex T end (TaTe) and heart rate-corrected TaTe (TaTec) were measured and considered to be representative of the whole depolarization process. QT dispersions (QTeD) and QTc dispersions (QTecD) were calculated to assess the degree of spatial inhomogeneity of action potential duration. RESULTS: Patients in group A had higher JT (272 +/- 36 ms versus 265 +/- 25 ms, P = 0.01), JTc (336 +/- 28 ms versus 318 +/- 18 ms, P = 0.01), JTa (210 +/- 28 ms versus 185 +/- 28 ms, P = 0.001) and JTac (240 +/- 20 ms versus 215 +/- 13 ms, P < 0.001) values than those of patients in group B, despite shorter TaTe (71 +/- 10 ms versus 90 +/- 18 ms, P < 0.001) and TaTec (88 +/- 12 ms versus 110 +/- 12 ms, P < 0.001). Moreover, QTeD and QTecD were significantly longer in group A than in group B (55 +/- 18 ms versus 42 +/- 19 ms [P = 0.01] and 80 +/- 18 ms versus 55 +/- 28 ms [P = 0.001], respectively). CONCLUSIONS: Patients with idiopathic VT exhibit inhomogeneous prolongation of ventricular repolarization, due to a considerable increase in the initial part in association with a shorter terminal phase, as well as a greater dispersion of ventricular repolarization.     

Effect of coronary angioplasty on precordial QT dispersion

Dispersion of the QT interval is a measure of inhomogeneity of ventricular repolarization. Because ischemia is associated with regional abnormalities of conduction and repolarization, we hypothesized that the surface electrocardiographic interval dispersion would increase in patients with symptomatic coronary artery disease in the absence of myocardial infarction and that successful revascularization would reduce QT interval dispersion. Thirty-seven consecutive patients with ischemia due to 1-vessel coronary artery disease without prior myocardial infarction who underwent percutaneous transluminal coronary angioplasty (PTCA) were evaluated. Standard 12-lead electrocardiograms were performed 24 hours before, 24 hours after, and late (>2 months) after PTCA. Precordial QT interval dispersions were determined from differences in the maximum and minimum corrected QT intervals. Mean QT interval dispersion before PTCA was 60 +/- 9 ms, immediately after PTCA 23 +/- 14 ms (p <0.001), and late after PTCA 29 +/- 18 ms (p <0.001 vs before PTCA). The shortest precordial QT interval increased immediately after PTCA (367 +/- 40 vs 391 +/- 39 ms; p <0.02) and then remained stable late after PTCA (376 +/- 36 ms, p = NS vs immediately after PTCA). Symptomatic recurrent ischemia in 8 patients with documented restenosis increased QT interval dispersion (56 +/- 15 ms [p <0.01] vs 25 +/- 14 ms immediately after PTCA), which decreased again after successful repeat PTCA (22 +/- 13 ms [p <0.01] vs before the second PTCA). QT interval dispersion decreases after successful coronary artery revascularization and increases with restenosis. Therefore, QT interval dispersion may be a marker of recurrent ischemia due to restenosis after PTCA.     

Effect of temperature on the reactivities of polyreactive and monospecific monoclonal IgG antibodies

To investigate possible sex differences in the dynamics of T wave generation, the maximum instantaneous slope of the ascending and descending limbs of the T wave (max dV/dt and min dV/dt, respectively), were calculated. These rate of repolarization parameters, as well as more traditional repolarization duration parameters (QT, JT, Q to T wave peak [QTm] and J to T wave peak [JTm]), were measured by computer using digitized electrocardiograms (ECGs) from the V5 lead in 562 normal subjects (443 men and 119 women; mean age 37 years), whose heart rates (HRs) were confined to one of three narrow ranges, namely 60 +/- 1, 70 +/- 1, or 80 +/- 1 beats/min. In both men and women, for each HR range absolute values of min dV/dt exceeded those of max dV/dt (P < .0001). However, absolute values of both max dV/dt and min dV/dt were consistently greater in men than in women for each HR range (P < .0001 at HR 60 +/- 1; P < .02 at HR 70 +/- 1, or 80 +/- 1). By using correlation analysis, max dV/dt and min dV/dt were shown to be independent of the repolarization duration variables (r < .30). Thus, whereas in both men and women the descending limb of the T wave is steeper than the ascending limb, the maximum slope of each limb of the T wave is steeper in men than in women. These findings add to a growing body of data indicating fundamental sex differences in the physiology of cardiac repolarization and propensity to torsade de pointes.     

The effects of a left bundle-branch block on ventricular repolarization dispersion

Patients with left bundle-branch block (LBBB) often present electrocardiographic abnormalities and, therefore, are excluded from studies concerning electrocardiographic evaluation of ventricular repolarization. The aim of the study was to assess whether LBBB could influence dispersion of ventricular repolarization. Surface electrocardiograms of 16 patients (9 males and 7 females, mean age 58 +/- 14 years) with episodes of intermittent LBBB were analyzed. Six patients were affected by coronary artery disease, 6 by hypertensive cardiomyopathy and 4 by dilated cardiomyopathy. Maximal QT and JT corrected intervals, QT and JT dispersion, and QT and JT dispersion corrected for heart rate, were obtained before and after LBBB. We observed a significant prolongation of maximal QT (412 +/- 29 vs 433 +/- 25 ms; p < 0.05), and of maximal corrected QT (457 +/- 37 vs 497 +/- 56 ms; p < 0.05) after LBBB. Maximal JT interval, also corrected for heart rate, did not show any significant modification after LBBB. Moreover, we did not observe any significant difference in electrocardiographic parameters of dispersion of repolarization. Our results seem to indicate that LBBB did not alter significantly dispersion of ventricular repolarization. QT dispersion is considered an important marker of risk for incidence of ventricular arrhythmias. If our results will be confirmed in larger groups of patients, analysis of QT dispersion could be extended even to patients with LBBB.     

The electrophysiological mechanism of the long QT syndrome

There are several functions to modulate if action potential prolongation and early and late after depolarizations are expected to appear, namely: calcium/sodium channels gating modes, potassium channels rectification, 3Na+/1Ca+2 exchange function, left/to/right balance of the sympathetic innervation of the heart. Based upon chronological correspondence of electrophysiological events and surface ecg waves, heterogeneous prolonged repolarization and after depolarizations are two possible explanations for QT interval prolongation and dispersion in both acquired and congenital long QT syndromes. Pauses commonly trigger arrhythmias in acquired LQTS, and imbalanced sympathetic drive commonly triggers arrhythmias in the congenital type of the syndrome.     

Effect of oral calcium loading on intact PTH and calcitriol in idiopathic renal calcium stone formers and healthy controls

The calciuric response after an oral calcium load (1000 mg elemental calcium together with a standard breakfast) was studied in 13 healthy male controls and 21 recurrent idiopathic renal calcium stone formers, 12 with hypercalciuria (UCa x V > 7.50 mmol/24 h) and nine with normocalciuria. In controls, serum 1,25(OH)2 vitamin D3 (calcitriol) remained unchanged 6 h after oral calcium load (50.6 +/- 5.1 versus 50.9 +/- 5.0 pg/ml), whereas it tended to increase in hypercalciuric (from 53.6 +/- 3.2 to 60.6 +/- 5.4 pg/ml, P = 0.182) and fell in normocalciuric stone formers (from 45.9 +/- 2.6 to 38.1 +/- 3.3 pg/ml, P = 0.011). The total amount of urinary calcium excreted after OCL was 2.50 +/- 0.20 mmol in controls, 2.27 +/- 0.27 mmol in normocalciuric and 3.62 +/- 0.32 mmol in hypercalciuric stone formers (P = 0.005 versus controls and normocalciuric stone formers respectively); it positively correlated with serum calcitriol 6 h after calcium load (r = 0.392, P = 0.024). Maximum increase in urinary calcium excretion rate, delta Ca-Emax, was inversely related to intact PTH levels in the first 4 h after calcium load, i.e. more pronounced PTH suppression predicted a steeper increase in urinary calcium excretion rate. Twenty-four-hour urine calcium excretion rate was inversely related to the ratio of delta calcitriol/deltaPTHmax after calcium load (r = -0.653, P = 0.0001), indicating that an abnormally up-regulated synthesis of calcitriol and consecutive relative PTH suppression induce hypercalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)     

Magnetocardiographic QT interval dispersion in postmyocardial infarction patients with sustained ventricular tachycardia: validation of automated QT measurements

QT dispersion is a measure of heterogeneity in ventricular repolarization. Increased ECG QT dispersion is associated with life-threatening ventricular arrhythmias. We studied if magnetocardiographic (MCG) measures of QT dispersion can separate postmyocardial infarction patients with and without susceptibility to sustained VT. Manual dispersion measurements were compared to a newly adapted automatic QT interval analysis method. Ten patients with a history of sustained VT (VT group) and eight patients without ventricular arrhythmias (Controls) were studied after a remote myocardial infarction. Single-channel MCGs were recorded from 42 locations over the frontal chest area and the signals were averaged. QT dispersion was defined as maximum-minimum or standard deviation of measured QT intervals. VT group showed significantly more QT and JT dispersion than Controls. QTapex dispersions were 127 +/- 26 versus 83 +/- 21 ms (P = 0.004) and QTend dispersions 130 +/- 37 versus 82 +/- 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QTapex and 27% for QTend dispersion on average. In conclusion, increased MCG QT interval dispersion seems to be associated with a susceptibility to VT in postmyocardial infarction patients. MCG mapping with automated QT interval analysis may provide a user independent method to detect nonhomogeneity in ventricular repolarization.     

Comparison of ECG variables of dispersion of ventricular repolarization with direct myocardial repolarization measurements in the human heart

INTRODUCTION: QT dispersion (QTD) from the 12-lead ECG has been widely adopted as a noninvasive index of dispersion of ventricular repolarization (DVR). QTD, however, has never been validated by direct comparison with myocardial DVR in the human heart. METHODS AND RESULTS: Monophasic action potential (MAP) recordings obtained in an earlier study were retrospectively matched with 12-lead ECGs available from within 24 hours of the invasive procedure. MAPs were available from an average of 8+/-3 left endocardial sites in 4 patients with left ventricular hypertrophy (LVH) and 7 patients with normal ECGs, and 6+/-2 epicardial sites in 3 patients of each group during normal ventricular activation. Local repolarization time (RT) was determined as MAP duration at 90% repolarization plus the local activation time. Dispersion of RT was calculated as the difference between the earliest and latest RT. ECGs were digitized and analyzed with recently described interactive QTD analysis software. In addition to standard QTD (defined as QTmax-QTmin), all currently proposed ECG dispersion variables were compared and correlated with the invasive measurements of DVR. QTD exhibited a reasonable correlation with dispersion of RT (R = 0.67; P < 0.01). Several other variables designed to measure DVR exhibited a similar, but not better, correlation. Among them, the QT peak/QT end ratio in V3 (R = -0.72; P < 0.01) and averaged over all analyzable leads (R = -0.59; P < 0.01) exhibited a good correlation with dispersion of RT, which was further improved when endocardial measurements were considered alone. T area measures did not correlate with dispersion of RT, but discriminated LVH. CONCLUSION: DVR can be assessed by means of a 12-lead surface ECG. Several of the variables under study exhibit a similar accuracy in determination of true myocardial dispersion of repolarization. Variables involving the terminal part of repolarization, such as the QT peak/QT ratio, even from a single lead, may add to the determination of DVR from the human heart.     

The practice of medical and surgical synovectomy: a UK survey

BACKGROUND: QT dispersion (QTd = QTmax-QTmin) measured as interlead variability of QT interval reflects the spatial inhomogeneity of ventricular repolarization times, and increased QTd may provide a substrate for malignant ventricular arrhythmias. Ischemia is associated with regional abnormalities of conduction and repolarization. HYPOTHESIS: This study aimed to investigate the effect of acute ischemia on QTd during successful percutaneous transluminal coronary angioplasty (PTCA). METHODS: Forty-three patients (10 women, 33 men, mean age 56 years) were enrolled in the study. Electrocardiogram (ECG) recordings were taken before PTCA and during balloon inflation period. QT maximum (QTmax), QT minimum (QTmin), and QTd (QTmax-QTmin) values were calculated from the surface ECG. RESULTS: There was no difference among QTmax values (p = 0.6). Mean QTmin during balloon inflation was lower than before PTCA (368 +/- 45 vs. 380 +/- 41 ms, p = 0.002). The difference between QTd values before and during balloon inflation was statistically important (65 +/- 9 vs. 76 +/- 10 ms, p = 0.001). This difference is caused by a decrease in QTmin during balloon inflation. CONCLUSION: Acute reversible myocardial ischemia induced by balloon inflation causes an increase in QTd value, and this increment is the result of a decrease in QTmin interval. Therefore, QTd may be a marker of reversible myocardial ischemia.     

Cardiac autonomic function and sensitivity to pain in postmenopausal women with angina and normal coronary arteries

An increased sensitivity to painful stimuli and an abnormal cardiac autonomic function have previously been reported in patients with angina and angiographically normal coronary arteries, a syndrome that mainly affects postmenopausal women. In this study we compared both general sensitivity to pain, by evaluating time to forearm ischemic pain (FIP) provoked by sphygmomanometer cuff inflation, and cardiac autonomic function, by measuring heart rate variability (HRV), and QT and QT(c) intervals on 24-hour Holter recordings, in 25 postmenopausal women with angina and normal coronary arteries and in 22 healthy postmenopausal women. Compared with controls, patients had a reproducible strikingly lower time to FIP (149 +/- 121 vs 295 +/- 158 seconds, p <0.001), whereas there were no differences between the 2 groups in HRV variables and mean 24-hour QT and QT(c) intervals. HRV indexes, and QT and QT(c) intervals also showed similar circadian patterns. Thus, our data show that postmenopausal women with angina and normal coronary arteries have an enhanced sensitivity to systemic painful stimuli, but no detectable impairment in cardiac autonomic function compared with a well-matched control group of postmenopausal healthy women.     

Effect of supplemental oxygen on supramaximal exercise performance and recovery in cystic fibrosis

The effects of supplemental O2 on recovery from supramaximal exercise and subsequent performance remain unknown. If recovery from exercise could be enhanced in individuals with chronic lung disease, subsequent supramaximal exercise performance could also be improved. Recovery from supramaximal exercise and subsequent supramaximal exercise performance were assessed after 10 min of breathing 100% O2 or room air (RA) in 17 cystic fibrosis (CF) patients [25 +/- 10 (SD) yr old, 53% men, forced expired volume in 1 s = 62 +/- 21% predicted] and 17 normal subjects (25 +/- 8 yr old, 59% men, forced expired volume in 1 s = 112 +/- 15% predicted). Supramaximal performance was assessed as the work of sustained bicycling at a load of 130% of the maximum load achieved during a graded maximal exercise. Peak minute ventilation (VE) and heart rate (HR) were lower in CF patients at the end of each supramaximal bout than in controls. In CF patients, single-exponential time decay constants indicated faster recovery of HR (tau HR = 86 +/- 8 and 73 +/- 6 s in RA and O2, respectively, P < 0.01). Similarly, fast and slow time constants of two-exponential equations providing the best fit for ventilatory recovery were improved in CF patients during O2 breathing (tau 1VE = 132.1 +/- 10.5 vs. 82.5 +/- 10.4 s; tau 2VE = 880.3 +/- 300.1 vs. 368.6 +/- 107.1 s, P < 0.01). However, no such improvements occurred in controls. Supramaximal performance after O2 improved in CF patients (109 +/- 6% of the 1st bout after O2 vs. 94 +/- 6% in RA, P < 0.01). O2 supplementation had no effect on subsequent performance in controls (97 +/- 3% in O2 vs. 93 +/- 3% in RA). We conclude that supplemental O2 after a short bout of supramaximal exercise accelerates recovery and preserves subsequent supramaximal performance in patients with CF.     

QT dispersion may be a useful adjunct for detection of myocardial infarction in the chest pain center

BACKGROUND: QT dispersion has been proposed as a noninvasive measurement of the degree of inhomogeneity in myocardial repolarization. Increased QT dispersion has been reported after myocardial infarction. We hypothesized that increased QT dispersion may be a useful adjunct for risk stratification in patients being evaluated in a chest pain center. METHODS AND RESULTS: Patients were admitted to the chest pain center for evaluation of chest pain. Exclusion criteria included (1) systolic blood pressure <90 mm Hg, (2) ischemia or infarction on the initial electrocardiograph (ECG), (3) elevated creatine kinase or MB fraction, and (4) chest pain associated with cocaine use. Serial creatine kinase and MB levels and ECGs were obtained at 0, 6, and 9 hours. Patients were monitored for (1) creatine kinase and MB rise, (2) ECG changes for infarction, (3) ST-segment changes, and (4) rest angina. A negative evaluation at the chest pain center led to an exercise stress test. Patients with a positive exercise stress test were admitted for further evaluation and patients with a negative exercise stress test result were discharged home. Patients were divided into 3 groups. Group 1 consisted of patients who were found to have an acute myocardial infarction (AMI), group 2 consisted of patients with prior history of coronary artery disease but no evidence of AMI, and group 3 consisted of patients without prior coronary artery disease or AMI. QT dispersion was measured on the initial ECG in all patients. A total of 586 patients were evaluated. Group 1 consisted of 13 patients with mean QT dispersion of 44.6+/-18.5 ms, group 2 consisted of 267 patients with a mean QT dispersion of 10.0+/-13.8 ms, and group 3 consisted of 303 patients with a mean QT dispersion of 10.5+/-10.0 ms. Analysis of variance showed a significantly higher QT dispersion in patients who had AMI compared with other patients with chest pain (P< .001). CONCLUSIONS: QT dispersion can be a useful diagnostic adjunct for detection of AMI in patients with chest pain with a normal ECG and normal cardiac enzymes.     

Surgical relevance of diagnostic imaging of abdominal tumors--decision making in pancreatic tumor

1. An association has been reported between QT interval abnormalities and cardiovascular autonomic neuropathy in diabetic patients. The QT interval abnormalities reflect local inhomogeneities of ventricular recovery time and may be related to an imbalance in cardiac sympathetic innervation. Sympathetic innervation of the heart can be visualized and quantified by single-photon emission-computed tomography with m-[123I]iodobenzylguanidine. In this study we evaluated cardiac sympathetic integrity by m-[123I]iodobenzylguanidine imaging and the relationship between both QT interval prolongation and QT dispersion from standard 12-lead ECG variables and m-[123I]iodobenzylguanidine uptake in insulin-dependent diabetic patients. 2. Three patient groups were studied, comprising six healthy control subjects, nine diabetic patients without cardiovascular autonomic neuropathy (CAN-) and 12 diabetic patients with cardiovascular neuropathy (CAN+). Resting 12-lead ECG was recorded for measurement of maximal QT interval and QT dispersion. The QT interval was heart rate corrected using Bazett's formula (QTc) and the Karjalainen approach (QTk). Quantitative measurement (in counts/min per g) and visual defect pattern of m-[123I]iodobenzylguanidine uptake were performed using m-[123I]iodobenzylguanidine single-photo emission-computed tomography. 3. Global myocardial m-[123I]iodobenzylguanidine uptake was significantly reduced in both diabetic patient groups compared with control subjects. The visual defect score of m-[123I]iodobenzylguanidine uptake was significantly higher in CAN+ diabetic patients than in control subjects and in CAN- patients. This score was not significantly different between control subjects and CAN- patients. QTc interval and QT dispersion were significantly increased in CAN+ diabetic patients as compared with control subjects (QTc: 432 +/- 15 ms versus 404 +/- 19 ms, P < 0.05; QT dispersion: 42 +/- 10 versus 28 +/- 8 ms, P < 0.05). QT dispersion was also significantly longer in CAN- diabetic patients than in control subjects (41 +/- 9 ms versus 28 +/- 8 ms, P < 0.05). QTc interval was significantly related to global myocardial m-[123I]iodobenzylguanidine uptake and defect score in diabetic patients (r = -0.648, P < 0.01, and r = 0.527, P < 0.05, respectively). There was no correlation between QT dispersion and both m-[123I]iodobenzylguanidine uptake measures. 4. In conclusion, these findings suggest that m-[123I]iodobenzylguanidine imaging is a valuable tool for the detection of early alterations in myocardial sympathetic innervation in long-term diabetic patients without cardiovascular autonomic neuropathy. Insulin-dependent diabetic patients with cardiovascular autonomic neuropathy have a delayed cardiac repolarization and increased variability of ventricular refractoriness. The cardiac sympathetic nervous system seems to be one of the determinants of QT interval lengthening, but does not appear to be involved in dispersion of ventricular recovery time. It is assumed that QT dispersion is based on more complex electrophysiological mechanisms which remain to be elucidated.     

Effects of quinidine on repolarization in canine epicardium, midmyocardium, and endocardium: II. In vivo study

BACKGROUND: In the companion article, we report a significant difference in quinidine effects on the action potential duration between surface (epicardial and endocardial) cells and midmyocardial cells (M cells) of canine left ventricle in vitro. This article considers two questions raised by the previous study: (1) Are the complex quinidine effects in vitro reflected in its actions on the heart in situ? (2) What are the cellular determinants of quinidine effects on QT interval in ECG? METHODS AND RESULTS: We used plunge and surface electrodes to measure activation-recovery intervals (ARIs) of bipolar electrograms obtained from epicardium, endocardium, and midmyocardium (3, 5, and 9 mm from epicardium) of canine left ventricle in conditions of AV block and right ventricular pacing. Quinidine was infused continuously; its plasma level increased from 1.6+/-0.1 microg/mL at 30 minutes to 7.6+/-0.7 microg/mL at 180 minutes. At cycle lengths (CLs) from 300 to 1500 ms, there was no ARI gradient across the ventricular wall before and during quinidine infusion. At a CL of 300 ms, therapeutic concentrations of quinidine prolonged ARIs and QT intervals. At a CL of 1500 ms, ARIs were significantly prolonged at low quinidine concentrations. With an increase of quinidine concentration, this effect subsided and disappeared. CONCLUSIONS: In situ, quinidine-induced prolongation of repolarization is uniform in all myocardial layers and follows the pattern observed in M cells in vitro. The ability of quinidine in therapeutic concentrations to prolong repolarization at rapid heart rates can contribute to its antiarrhythmic efficacy.     

Liquefied aftercataract: a complication of continuous curvilinear capsulorhexis and intraocular lens implantation in the lens capsule

OBJECTIVE: To compare effects of N(G)-monomethyl-L-arginine (L-NMMA; a NO synthase inhibitor) and L-arginine (a NO synthase substrate) on haemodynamics in healthy men at rest and during exercise. METHODS: We infused L-NMMA and saline placebo intravenously in two groups of eight healthy men. Each group underwent a two-phase, randomized, single-blind crossover study. Men in one group received 3 mg/kg L-NMMA and men in the other group received 6 mg/kg L-NMMA. Haemodynamic measurements were performed before, during and after a 12 min stepped exercise protocol starting 6 min after the intravenous infusion. A further six men received, according to the same study design, 30 g L-arginine over 30 min and saline placebo before exercise. Blood pressure was measured by sphygmomanometry and cardiac output by bioimpedance, allowing computation of total systemic vascular resistance index (SVRI). RESULTS: Infusion of 6 mg/kg L-NMMA into men at rest produced modest increases (compared with effect of saline placebo) in systolic and diastolic blood pressures of 4.1 +/- 1.1 and 12.6 +/- 3.5%, respectively (means +/- SEM, P < 0.01 for both comparisons) and a marked increase in SVRI of 39.2 +/- 5.2% (P < 0.01). Cardiac index and heart rate were 22.0 +/- 3.3 and 17.0 +/- 4.4% lower after administration of L-NMMA (P < 0.01 for each comparison) than after infusion of saline placebo. During exercise there was no significant difference between total SVRI after infusions of L-NMMA and saline (difference not significant, diminished with increasing exercise). Six minutes into recovery the difference between total SVRI after infusions of L-NMMA and saline reappeared with SVRI 25 +/- 6.9% higher after infusion of L-NMMA than after infusion of saline (P < 0.01). Administration of L-arginine had no significant effect on haemodynamics in men at rest, during exercise and during recovery. CONCLUSIONS: Effects of L-NMMA on total systemic vascular resistance during exercise are less marked than are those on subjects at rest, probably because vasodilatation of resistance vessels of skeletal muscle during exercise is mediated mainly by factors other than NO. Our results also suggest that NO synthesis in healthy men is not substrate limited either at rest or during exercise.     

Congenital long QT syndrome

The long QT syndrome (LQTS) combines a prolonged QT interval with an enhanced risk of polymorphous ventricular arrhythmias that may lead to syncope and sudden cardiac death. It may be congenital or acquired (the latter sometimes caused by drugs). Congenital LQTS is a rare disease, usually discovered during the clinical evaluation of understood syncopes or at cardiological examination after an unexpected sudden cardiac death of a close relative. The syncope frequently occurs during physical exercise, fear or sudden loud noises. In patients with symptomatic LQTS, the mortality 10 years after the first syncope amounts to approximately 50%. A prolonged QT interval indicates abnormal repolarization or deceleration of the depolarization. An increase of the sympathetic tone, e.g. during physical exercise and emotions, causes prolongation of the QT interval. Congenital LQTS has been associated with genetic mutations, for instance on chromosomes 3 and 7. Treatment consists af administration of beta-blockers, sympathectomy and, if necessary, implantation of an automatic cardioverter/defibrillator.     

Training effects of short and long bouts of brisk walking in sedentary women

This study compared the effects of short and long bouts of brisk walking in sedentary women. Forty seven women aged 44.4 +/- 6.2 yr (mean +/- SD) were randomly assigned to either three 10-min walks per day (short bouts), one 30-min walk per day (long bouts) or no training (control). Brisk walking was done on 5 d x wk(-1), at 70 to 80% of maximal heart rate, typically at speeds between 1.6 and 1.8 m x s(-1) (3.5 and 4.0 mph), for 10 wk. Subjects agreed not to make changes to their diet. Twelve short-bout walkers, 12 long-bout walkers, and 10 controls completed the study. Relative to controls, VO2max (short-bout, +2.3 +/- 0.1 mL x kg(-1) x min(-1); long-bout, +2.4 +/- 0.1 mL x kg(-1) x min(-1); controls, -0.5 +/- 0.1 mL x kg(-1) x min[-1]) and the VO2 at a blood lactate concentration of 2 mmol x L(-1) increased in walkers (both P < 0.05), with no difference in response between walking groups. Neither heart rate during standard, submaximal exercise nor resting systolic blood pressure changed in a different way in walkers and controls. The sum of four skinfold thicknesses decreased in both walking groups (P < 0.05) but body mass (short-bout, -1.7 +/- 1.7 kg; long-bout, -0.9 +/- 2.0 kg; controls, +0.6 +/- 0.7 kg) and waist circumference decreased significantly only in short-bout walkers. Changes in anthropometric variables did not differ between short- and long-bout walkers. Thus short bouts of brisk walking resulted in similar improvements in fitness and were at least as effective in decreasing body fatness as long bouts of the same total duration.     

Augmented exercise plasma noradrenaline with impaired chronotropic responsiveness in patients with hypertrophic cardiomyopathy

1. There is controversy regarding plasma catecholamine levels in patients with hypertrophic cardiomyopathy (HCM) and few data exist on serial plasma catecholamine measurements during exercise. The present study determined whether cardiovascular and plasma catecholamine responses to exercise were altered in patients with HCM. 2. Plasma noradrenaline (NA) and adrenaline were measured at rest, at the end of each stage during exercise and immediately and 5 min after submaximal treadmill exercise in 15 patients with non-obstructive HCM (13 males, two females; mean (+/- SEM) age 54 +/- 3 years) and in 15 age- and sex-matched controls. The ratio of the increment in heart rate (HR) divided by the increment in plasma NA during exercise (delta HR/delta NA) was used as an index of chronotropic sympathetic responsiveness to exercise. 3. Exercise duration was shorter (11.2 +/- 0.6 vs 8.7 +/- 0.6 min for control vs HCM, respectively; P < 0.01) and diastolic blood pressure was significantly higher at stages I and II of modified Bruce protocol HCM. 4. Resting plasma NA levels (149 +/- 17 vs 167 +/- 28 pg/mL for control vs HCM, respectively; NS) were not different, but plasma NA levels at stages I and II were significantly higher in HCM than in controls (243 +/- 26 vs 399 +/- 69 pg/mL (P < 0.05) and 308 +/- 30 vs 548 +/- 110 pg/mL (P < 0.05), respectively). 5. Peak plasma NA levels were not significantly higher in HCM than in controls (578 +/- 59 vs 918 +/- 184 pg/mL, respectively; NS). 6. The ratio delta HR/delta NA was significantly lower in HCM compared with control at stages I and II (0.49 +/- 0.10 vs 0.21 +/- 0.05 (P < 0.05) and 0.38 +/- 0.06 vs 0.20 +/- 0.05 (P < 0.05), respectively). There were no differences in plasma adrenaline responses during exercise between the two groups. 7. Patients with HCM had augmented plasma NA levels during submaximal exercise with a higher diastolic blood pressure response. Chronotropic sympathetic responsiveness was impaired during the early stages of exercise in patients with HCM.     

Heparinized saline or normal saline as a flush solution in intermittent intravenous lines in infants and children

Physical exertions are related to sudden cardiac death following acute myocardial infarction (AMI). Abnormalities in the autonomic modulation during exercise were noted in animals with AMI that were susceptible to potentially lethal arrhythmias. This study was done to evaluate the changes in the autonomic activity during exercise and recovery in AMI patients with good exercise capacity, using spectral analysis of R-R intervals of electrocardiogram (ECG). Symptom-limited treadmill exercise test was done on 17 patients of AMI with mild heart failure (in 7-10 days after the attack) and 21 healthy controls. The exercise was divided into 7 stages; rest, early exercise, mid-exercise, peak exercise, early recovery, mid-recovery, and late recovery. Power spectral analysis of R-R intervals of ECG was performed for each stage. Low frequency (0.04-0.15 Hz) and high frequency (0.15-0.40 Hz) powers, and their ratio were obtained. These parameters were observed throughout the stages in both groups. The trend of their changes during exercise and recovery was essentially the same for both groups; high and low frequency powers progressively decreased during exercise and abruptly increased during early recovery, but did not return to the values at those of rest until 9 minutes into the recovery. When the parameters were compared between the groups, there was a significantly greater decrease of high frequency power during the early exercise (p < 0.05), and a higher ratio of low to high frequency power during the early recovery (p < 0.05) in the patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Precordial QT dispersion and inducible ventricular tachycardia

We compared the performance of precordial QT dispersion, late potentials on the signal-averaged electrocardiogram (ECG), and reduced left ventricular ejection fraction for identification of inducible ventricular tachycardia (VT) in 162 patients undergoing electrophysiologic study (EPS). QT(apex) dispersion in 56 patients with inducible VT (72 +/- 55 msec) was greater than that in 106 patients without inducible VT (55 +/- 36 msec, p < 0.01); dispersion was greater in both groups than in 144 normal subjects (33 +/- 19 msec). A QT(apex) dispersion partition of more than 68 msec, the upper ninety-fifth percentile in normal subjects, identified inducible VT with a specificity of 75% and a sensitivity of 45%. Although the performances of late potentials (specificity 82%, sensitivity 59%) and reduced ejection fraction (specificity 86%, sensitivity 54%) were each stronger than QT dispersion alone for identification of inducible VT, abnormal QT(apex) dispersion remained a significant additional predictor of inducible VT in a logistic regression model that included the three variables (specificity 78%, sensitivity 75%).