Body surface distribution and response to drugs of ST segment elevation in Brugada syndrome: clinical implication of eighty-seven-lead body surface potential mapping and its application to twelve-lead electrocardiograms

INTRODUCTION: Body surface distribution and magnitude of ST segment elevation and their reflection in 12-lead ECGs have not been clarified in Brugada syndrome. METHODS AND RESULTS: Eighty-seven-lead body surface potential mapping and 12-lead ECGs were recorded simultaneously in 25 patients with Brugada syndrome and 40 control patients. The amplitude of the ST segment 20 msec after the end of QRS (ST20) was measured from all 87 leads, and an ST isopotential map was constructed. The maximum ST elevation (maxST20) was distributed in an area of the right ventricular outflow tract in all Brugada patients, and it was larger than that in control patients (0.37 +/- 0.13 vs 0.12 +/- 0.04 mV; P < 0.0005). The maximum was observed on the level of the parasternal fourth intercostal space, on which the V1 and V2 leads of the standard 12-lead ECG were located, in 18 of the 25 Brugada patients in whom typical coved- or saddleback-type ST elevation was seen in leads V1 and V2. The maximum was located on the second intercostal space in the remaining seven Brugada patients in whom only a mild saddleback-type ST elevation was seen in leads V1 and V2 of the 12-lead ECG. Typical ST segment elevation was recognized in leads V1 and V2, which were recorded on the second or third intercostal space. ST elevation in Brugada patients was dramatically normalized by isoproterenol, a beta-adrenergic agonist (maxST20 = 0.17 +/- 0.08 mV; P < 0.0005 vs control conditions), and accentuated by disopyramide, an Na+ channel blocker (maxST20 = 0.50 +/- 0.15 mV; P < 0.0005 vs control conditions), without any change in the location of the maxST20. CONCLUSION: Our data indicate that recordings of leads V1-V3 of the 12-lead ECG on the parasternal second or third intercostal space would be helpful in diagnosing suspected patients with Brugada syndrome. The data suggest that Na+ channel blockers are capable of accentuating ST elevation in leads V1-V3.     

Electrocardiographic alterations in leads V1 to V3 in the diagnosis of right and left ventricular infarction

As Q wave and ST segment elevation in leads V1 to V3 may be due either to right ventricular infarction (RVI) or to anterior left ventricular infarction (ALVI), 72 autopsy patients with acute myocardial infarction who had had conventional 12-lead ECG records were studied to determine the accuracy of these ECG criteria, both for the diagnosis of RVI (29 patients, group A) and of ALVI (43 patients, group B). The accuracy of three ECG criteria (Q wave, ST segment elevation greater than or equal to 0.05 mV, and ST segment elevation greater than or equal to 0.1 mV) in diagnosing group A and group B patients was determined in each precordial lead (V1, V2, and V3) and the three criteria were found to be significantly more accurate in diagnosing group B than group A patients. In conclusion, although Q wave and ST segment elevation in leads V1, V2, and V3 may be present in some cases of RVI, their accuracy is too low to be considered useful diagnostic criteria in these patients.     

Assessment of left ventricular performance during percutaneous transluminal coronary angioplasty: a study by intravenous digital subtraction ventriculography.

Left ventricular performance during percutaneous transluminal coronary angioplasty was assessed in 52 patients by intravenous digital subtraction ventriculography. After injection of contrast into the right atrium ventriculograms were obtained before and during balloon inflation. In 37 patients they were also obtained after the procedure. A 12 lead electrocardiogram was monitored throughout. During balloon inflation the left ventricular ejection fraction fell (from 73% to 57%) in all but one patient; the decreases in patients with single vessel or multivessel disease were similar. The fall in left ventricular ejection fraction during percutaneous transluminal coronary angioplasty of the left anterior descending artery (19%) was significantly greater than that during balloon inflation in the right coronary (10%) or circumflex (8%) coronary arteries. It also reduced anterobasal, anterior, and apical segmental shortening while right coronary percutaneous transluminal coronary angioplasty affected inferior and apical segments. In 33 (63%) patients the ST segment was altered during balloon inflation. The fall in left ventricular ejection fraction correlated significantly with the magnitude of both ST segment elevation (r = 0.637) and ST depression (r = 0.396). Left ventricular ejection fraction and regional wall motion returned to baseline values after the procedure. Balloon inflation during percutaneous transluminal coronary angioplasty produces considerable abnormalities of global and regional left ventricular performance and this indicates the presence of myocardial ischaemia, which may not be apparent on electrocardiographic monitoring. Intravenous digital subtraction ventriculography is useful for monitoring left ventricular performance during controlled episodes of coronary occlusion produced by balloon inflation.     

Assessment of left ventricular performance during percutaneous transluminal coronary angioplasty: a study by intravenous digital subtraction ventriculography

Left ventricular performance during percutaneous transluminal coronary angioplasty was assessed in 52 patients by intravenous digital subtraction ventriculography. After injection of contrast into the right atrium ventriculograms were obtained before and during balloon inflation. In 37 patients they were also obtained after the procedure. A 12 lead electrocardiogram was monitored throughout. During balloon inflation the left ventricular ejection fraction fell (from 73% to 57%) in all but one patient; the decreases in patients with single vessel or multivessel disease were similar. The fall in left ventricular ejection fraction during percutaneous transluminal coronary angioplasty of the left anterior descending artery (19%) was significantly greater than that during balloon inflation in the right coronary (10%) or circumflex (8%) coronary arteries. It also reduced anterobasal, anterior, and apical segmental shortening while right coronary percutaneous transluminal coronary angioplasty affected inferior and apical segments. In 33 (63%) patients the ST segment was altered during balloon inflation. The fall in left ventricular ejection fraction correlated significantly with the magnitude of both ST segment elevation (r = 0.637) and ST depression (r = 0.396). Left ventricular ejection fraction and regional wall motion returned to baseline values after the procedure. Balloon inflation during percutaneous transluminal coronary angioplasty produces considerable abnormalities of global and regional left ventricular performance and this indicates the presence of myocardial ischaemia, which may not be apparent on electrocardiographic monitoring. Intravenous digital subtraction ventriculography is useful for monitoring left ventricular performance during controlled episodes of coronary occlusion produced by balloon inflation.     

Body surface area of ST elevation and the presence of late potentials correlate to the inducibility of ventricular tachyarrhythmias in Brugada syndrome

INTRODUCTION: The value of noninvasive markers reflecting repolarization and/or conduction abnormalities in identifying patients with abnormal ECG showing a pattern of atypical right bundle branch block and ST elevation syndrome (Brugada syndrome) at risk for life-threatening arrhythmias is controversial. Because right precordial ST elevation reflects inhomogeneous repolarization, we hypothesized that a correlation between the area of ST elevation, that is, the area of inhomogeneous repolarization, and the inducibility of ventricular tachyarrhythmias (VT) exists. Therefore, the body surface area of ST elevation and the presence of late potentials were compared to the inducibility of VT in patients with the characteristic ECG of Brugada syndrome. METHODS AND RESULTS: A 120-channel body surface potential map was recorded at rest and after administration of a Class I agent (ajmaline, 1 mg/kg) to measure the body surface area of ST elevation (> or = 0.2 mV) in 23 individuals (16 patients had been resuscitated from near sudden cardiac death or had suffered syncope) with an ECG compatible with the diagnosis of Brugada syndrome as well as in 15 healthy controls and in 15 patients with arrhythmogenic right ventricular cardiomyopathy. Late potentials were assessed in 20 of the Brugada patients using signal-averaged ECG. Programmed ventricular stimulation was performed at two ventricular sites with up to three extrastimuli. Mean body surface area of ST elevation (> or = 0.2 mV) of all Brugada syndrome patients was 154 +/- 139 cm2 (control 9 +/- 9 cm2; P < 0.001). In the group of patients with arrhythmogenic right ventricular cardiomyopathy, only one patient was found to have an area of ST elevation (165 cm2). In the presence of ajmaline, area size increased to 330 +/- 223 cm2 in Brugada syndrome patients (P < 0.05). In patients with inducible sustained (n = 15) and nonsustained VT (n = 3), a mean area of 183 +/- 139 cm2 was found, whereas the area was only 52 +/- 58 cm2 in those with no VT induction (P < 0.05). For an area > or = 50 cm2, there were positive and negative predictive values of 92% and 60%, respectively. Positive late potentials were found in 60% of patients and correlated to the inducibility during programmed ventricular stimulation (positive predictive value 100%, negative predictive value 75%; P < 0.001). CONCLUSION: In patients with Brugada syndrome, the body surface area of ST elevation and the presence of late potentials correlate to the inducibility of VT during programmed ventricular stimulation and may be of value as a new noninvasive marker for risk stratification in these patients.     

Electrocardiographic predictors of Brugada type response during Na channel blockade challenge.

AIM: To identify ECG predictors of Brugada type response during Na channel blockade challenge. METHODS: We studied prospectively 103 patients (M = 76, 45 +/- 13 years) in whom ECGs were collected during ajmaline challenge. ECG recordings included the high right precordial leads (-2V(1) and -2V(2)). A positive response was defined by a >0.2 mV J point or ST segment elevation and a down-sloping pattern of the ST segment in at least one right precordial lead. RESULTS: Ajmaline challenge was positive in 48 (47%) of the 103 cases. Baseline J wave elevation was greater in -2V(1) (0.077 +/- 0.078 mV vs. 0.038 +/- 0.046 mV, P = 0.003) and -2V(2) (0.149 +/- 0.103 mV vs. 0.043 +/- 0.088 mV, P < 0.001) in cases with a subsequent positive response. In contrast, ST segment elevation and T wave amplitudes were reduced in V(1), V(2) and V(3). Logistic regression showed that J wave elevation in -2V(2) and decreased T wave amplitude in V(3) at baseline were independent predictors of a positive response. Baseline J wave elevation >0.16 mV in -2V(2) had a specificity of 100%, a sensitivity of 40%, a positive predictive value of 100% and a negative predictive value of 28%. CONCLUSION: J wave elevation >0.16 mV in -2V(2) was the strongest predictor of a Brugada type response to Na channel blockade challenge when Brugada syndrome was suspected on a baseline ECG.     

Early continuous ST segment monitoring in unstable angina: prognostic value additional to the clinical characteristics and the admission electrocardiogram.

BACKGROUND AND OBJECTIVE: In unstable angina, clinical characteristics, resting electrocardiography, and early continuous ST segment monitoring have been individually reported to identify subgroups at increased risk of adverse outcome. It is not known, however, whether continuous ST monitoring provides additional prognostic information in such a setting. DESIGN: Observational study of 212 patients with unstable angina without evidence of acute myocardial infarction admitted to district general hospitals, who had participated in a randomised study comparing heparin and aspirin treatment versus aspirin alone. METHODS: Clinical variables and a 12 lead electrocardiogram (ECG) were recorded at admission, and treatment was standardised to include aspirin, atenolol, diltiazem, and intravenous glyceryl trinitrate, in addition to intravenous heparin (randomised treatment). Continuous ST segment monitoring was performed for 48 h and all inhospital adverse events were recorded. RESULTS: The admission ECG was normal in 61 patients (29%), showed ST depression in 59 (28%) (17 > or = 0.1 mV), and T wave changes in a further 69 (33%). The remaining 23 had Q waves (18), right bundle branch block (four), or ST elevation (one). During 8963 h of continuous ST segment monitoring (mean 42.3 h/patient), 132 episodes of transient myocardial ischaemia (104 silent) were recorded in 32 patients (15%). Forty patients (19%) had an adverse event (cardiac deaths (n = 3), non-fatal myocardial infarction (n = 6) and, emergency revascularisation (n = 31)). Both admission ECG ST depression (P = 0.02), and transient ischaemia (P < 0.001) predicted an increased risk of non-fatal myocardial infarction or death, while no patients with a normal ECG died or had a myocardial infarction. Adverse outcome was predicted by admission ECG ST depression (regardless of severity) (odds ratio (OR) 3.41) (P < 0.001), and maintenance beta blocker treatment (OR 2.95) (P < 0.01). A normal ECG predicted a favourable outcome (OR 0.38) (P = 0.04), while T wave or other ECG changes were not predictive of outcome. Transient ischaemia was the strongest predictor of adverse prognosis (OR 4.61) (P < 0.001), retaining independent predictive value in multivariate analysis (OR 2.94) (P = 0.03), as did maintenance beta blocker treatment (OR 2.85) (P = 0.01) and admission ECG ST depression, which showed a trend towards independent predictive value (OR 2.11) (P = 0.076). CONCLUSIONS: Patients with unstable angina and a normal admission ECG have a good prognosis, while ST segment depression predicts an adverse outcome. Transient myocardial ischaemia detected by continuous ST segment monitoring in such patients receiving optimal medical treatment provides prognostic information additional to that gleaned from the clinical characteristics or the admission ECG.     

Comparison of diagnostic accuracy, time dependency, and prognostic impact of abnormal Q waves, combined electrocardiographic criteria, and ST segment abnormalities in right ventricular infarction.

OBJECTIVE--To determine the diagnostic and prognostic impact of abnormal Q waves in comparison to or in combination with ST segment abnormalities in the right precordial and inferior leads as indicators of right ventricular infarction during the acute phase of inferior myocardial infarction. DESIGN--Prospective study of a consecutive series of 200 patients with acute inferior myocardial infarction with and without right ventricular infarction. SETTING--Department of internal medicine, university clinic. RESULTS--Right ventricular infarction was diagnosed in 106 (57%) out of 187 patients from the results of coronary angiography, technetium pyrophosphate scanning, and measurement of haemodynamic variables or at necropsy, or both. In the acute phase of inferior infarction ST segment elevation > or = 0.1 mV in any of the right precordial leads V4-6R was the most reliable criterion for right ventricular infarction (sensitivity, 89%; specificity, 83%). Abnormal Q waves in the right precordial leads, the most specific criterion (91%) for right ventricular infarction, were superior to ST segment elevation in patients admitted > 12 hours after the onset of symptoms. Both ST segment elevation in leads V4-6R (increase in in hospital mortality, 6.2-times; P < 0.001; major complications, 2.3-times; P < 0.01) and abnormal Q waves (2.3-times, P < 0.05; 1.8-times, P < 0.05) on admission were highly predictive of a worse outcome during the in hospital period. In the presence of inferior myocardial infarction previously proposed combined electrocardiographic criteria were not better diagnostically or prognostically than ST segment abnormalities and abnormal Q waves alone. CONCLUSIONS--During the first 24 hours of inferior myocardial infarction ST segment elevation and abnormal Q waves derived from the right precordial leads are complementary rather than competitive criteria for reliably diagnosing right ventricular infarction, both indicating a worse in hospital course for the patient. In this they are better than any other previously proposed combined electrocardiographic criteria in diagnosing right ventricular infarction. Right precordial leads should be routinely monitored in acute inferior myocardial infarction.     

Acute electrocardiographic changes associated with successful coronary thrombolysis in acute myocardial infarction

In this study ECG changes were analyzed to assess the acute effects of antegrade blood flow on the ECG in patients with AMI. The study population consisted of 22 patients with MI in whom the totally occluded left anterior descending artery (LAD) or right coronary artery (RCA) was recanalized by intracoronary urokinase infusion (recanalized group) and 14 patients in whom the occluded coronary artery was not successfully recanalized (control group). No significant difference was found in the sum of ST segment elevation (V2-V4 leads for the LAD-occluded group, II, III and aVF leads for the RCA-occluded group) before urokinase infusion. In the recanalized group sigma ST abruptly increased in 5 min after recanalization in 13 of 16 LAD-occluded patients from 1.49 +/- 0.89 mV to 2.44 +/- 1.67 mV (p less than 0.005), and in 4 of 6 RCA-occluded patients from 0.66 +/- 0.12 mV to 1.42 +/- 0.52 mV (p less than 0.01). However increased sigma ST in the recanalized group was reduced to the control value existing before recanalization within 30 min after recanalization and continued to decline more rapidly than in the control group. These transient ST segment elevations were not correlated with long-term angiographic determinants of left ventricular function. We conclude that ST segment shows abrupt augmentation after successful thrombolysis and that continuous ST segment monitoring is useful for assessing thrombolysis in AMI.     

Is the development of myocardial tolerance to repeated ischemia in humans due to preconditioning or to collateral recruitment?

OBJECTIVES: The purpose of this study in patients with quantitatively determined, poorly developed coronary collaterals was to assess the contribution of ischemic as well as adenosine-induced preconditioning and of collateral recruitment to the development of tolerance against repetitive myocardial ischemia. BACKGROUND: The development of myocardial tolerance to repeated ischemia is nowadays interpreted to be due to biochemical adaptation (i.e., ischemic preconditioning). METHODS: In 30 patients undergoing percutaneous transluminal coronary angioplasty, myocardial adaptation to ischemia was measured using intracoronary (i.c.) electrocardiographic (ECG) ST segment elevation changes obtained from a 0.014-in. (0.036 cm) pressure guidewire positioned distal to the stenosis during three subsequent 2-min balloon occlusions. Simultaneously, an i.c. pressure-derived collateral flow index (CFI, no unit) was determined as the ratio between distal occlusive minus central venous pressure divided by the mean aortic minus central venous pressure. The study patients were divided into two groups according to the pretreatment with i.c. adenosine (2.4 mg/min for 10 min starting 20 min before the first occlusion, n = 15) or with normal saline (control group, n = 15). RESULTS: Collateral flow index at the first occlusion was not different between the groups (0.15 +/- 0.10 in the adenosine group and 0.13 +/- 0.11 in the control group, p = NS), and it increased significantly and similarly to 0.20 +/- 0.14 and to 0.19 +/- 0.10, respectively (p < 0.01) during the third occlusion. The i.c. ECG ST elevation (normalized for the QRS amplitude) was not different between the two groups at the first occlusion (0.25 +/- 0.13 in the adenosine group, 0.25 +/- 0.19 in the control group). It decreased significantly during subsequent coronary occlusions to 0.20 +/- 0.15 and to 0.17 +/- 0.13, respectively. There was a correlation between the change in CFI (first to third occlusion; deltaCFI) and the respective ST elevation shift (deltaST): deltaST = -0.02 to 0.78 x deltaCFI; r = 0.54, p = 0.02. CONCLUSIONS: Even in patients with few coronary collaterals, the myocardial adaptation to repetitive ischemia is closely related to collateral recruitment. Pharmacologic preconditioning using a treatment with i.c. adenosine before angioplasty does not occur. The variable responses of ECG signs of ischemic adaptation to collateral channel opening suggest that ischemic preconditioning is a relevant factor in the development of ischemic tolerance.     

Proportion and prognosis of healthy people with coved or saddle-back type ST segment elevation in the right precordial leads during 10 years follow-up.

AIMS: The aim of this study was to investigate long-term proportion and prognosis of healthy subjects with right precordial ST segment elevation without family history of sudden death. METHODS AND RESULTS: We followed up electrocardiograms (ECGs) of 3339 healthy subjects (male/female 2646/693) who underwent periodical medical examination form 1992 to 2001 to determine the relationship between year-to-year changes of ST segment morphology and the risk of fatal arrhythmias. Inclusion criterion was defined as presenting either coved or saddle back type ST segment elevation (>0.2 mV) in the right precordial leads. The cumulative total subjects who showed Brugada-like ECG changes at least once throughout the follow-up period were 69 (male/female 67/2; age 47.9+/-8.9 years, 2.1% of total subjects). During a follow-up period, annual mean proportion of coved or saddle back type ST elevation in the right precordial leads was 1.22+/-0.23% (0.88-1.88%). The morphological pattern of ST segment elevation was saddle-back in 77.3+/-7.9% and coved in 22.7+/-7.9% of subjects. Throughout the follow-up period, 39 subjects (56.5%) showed changes in ST segment elevation pattern. Twenty-nine subjects (42.0%) showed normalization of ST segment elevation at least once. Sixty-nine subjects were followed for a period of one to 10 years (median 4 years, interquartile range 4-8 years). Only one subject with persistent saddle-back type ST elevation had episodes of ventricular fibrillation (VF). CONCLUSIONS: The average proportion of healthy subject who had coved or saddle-back type of ST elevation in the right precordial leads without family history of sudden death was 1.22% and the risk of fatal arrhythmias was low (1/393.5 subject-years).     

The value of the intracoronary electrogram for the early detection of myocardial ischaemia during coronary angioplasty.

The clinical value of intracoronary electrography for the detection of myocardia ischaemia was assessed during coronary angioplasty and compared to a standard technique of surface ECG monitoring. In 73 patients undergoing single lesion angioplasty, an intracoronary electrogram and four representative surface ECG leads were obtained. During angioplasty of the left anterior descending artery leads, I, V3, V5, V6 were recorded. For the circumflex artery leads I, aVL, aVF, V6, and for the right coronary artery leads II, III, aVF, V6 were monitored. Eight patients were excluded due to transient intraventricular conduction disturbances during balloon inflation; 65 patients remained for further analysis. Out of a total of 154 balloon inflations (35 in the circumflex, 71 in the left anterior descending and 48 in the right coronary artery), the percentage that produced a greater than or equal to 1 mm ST segment elevation, the time to the appearance of a greater than or equal to 1 mm ST segment elevation and the maximal ST segment elevation were recorded. During inflations in the circumflex artery, the respective values of these three parameters were 20%, 22.6 +/- 11.5 s and 0.37 +/- 0.80 mm in V6, the most sensitive surface lead, versus 70% (P less than 0.001), 14.4 +/- 9.6 s (P less than 0.01) and 5.82 +/- 6.35 mm (P less than 0.0001) on the intracoronary electrogram.(ABSTRACT TRUNCATED AT 250 WORDS)     

The impact of autoperfusion on quantitative electrocardiographic parameters of ischemia severity, extent, and "burden" during salvage of elective coronary angioplasty

Long angioplasty inflations have been reported using an autoperfusion system that delivers oxygenated blood distal to the balloon segment. The safety and efficacy of this system has been demonstrated in anatomically selected patients. The clinical use, however, is frequently to stabilize intimal dissection in unselected patients. We reviewed 12-lead continuous electrocardiographic (ECG) recordings in 40 patients in whom prolonged salvage with autoperfusion was attempted. Sub-optimal results were stabilized in 36 of 40, while 4 patients had urgent bypass. The presence of ischemia, as > or = 100 uV ST elevation over the 12 lead ECG, and the total ST deviation over all leads over the entire inflation period (total ischemic "burden") were compared within each patient between the longest standard balloon and autoperfusion inflations. Median duration of inflation was 3.03 min. with balloon vs. 15.6 min. with autoperfusion (p < 0.00002). Of the 40 patients, 35 (87%) had ECG ischemia with balloon vs. 18 (45%) with autoperfusion (p < .00002). Median severity of peak ST deviation was 321 uV with balloon vs. 132 uV with autoperfusion (p = 0.0001). Median extent of ST elevation was 3 leads with balloon vs. 0 leads with autoperfusion (p = 0.0001). Median total ischemic burden was similar with balloon (1173 uVmin) and autoperfusion (1083 uVmin, NS) despite the fivefold longer inflation duration with autoperfusion. Thus, in patients selected by clinical necessity rather than optimal anatomy, severity and extent of ST elevation were significantly reduced, although not entirely eliminated, by autoperfusion.     

Relationships between depolarization abnormality and repolarization abnormality in patients with Brugada syndrome: using body surface signal-averaged electrocardiography and body surface maps

INTRODUCTION: Repolarization and depolarization abnormalities have been reported to be related to Brugada syndrome. METHODS AND RESULTS: We evaluated the relationships between repolarization abnormality and depolarization abnormality using 48-lead unipolar signal-averaged electrocardiograms and 87-lead unipolar body surface maps in 15 patients with Brugada-type ECGs. Data were compared with those from healthy control subjects (n = 5) and within subgroups of Brugada syndrome with (n = 8) and without (n = 7) ventricular arrhythmias (VA) induced by programmed electrical stimulation (PES). Eighty-seven-lead body surface maps were recorded, and potential maps were constructed to evaluate elevation of the ST segment 20 ms after the J point. Forty-eight-lead signal-averaged ECGs were recorded, and isochronal maps of duration of the delayed potential (dDP) were constructed to evaluate the dDP in each lead. Potential maps showed that patients with Brugada-type ECG, especially those with VA induced by programmed electrical stimulation, had greater elevation of the ST segment in the right ventricular outflow tract, especially at E5. Isochronal maps of dDP in the Brugada-type ECG group showed that maximum dDP was located at E5 and that the area with long dDP was larger than that in the control subjects. The dDPs at E7, E5, F7, and F5 in the VA-inducible group were significantly longer than those in the VA-noninducible group. These results showed that the location of greater elevation in the ST segment coincided with the location of longer dDP. CONCLUSION: Repolarization abnormality and depolarization abnormality in the walls of both ventricles, especially in the right ventricular outflow tract, are related to the VA of Brugada syndrome.     

Effect of ischemia on implantable defibrillator intracardiac shock electrograms

Introduction: Few attempts have been made to extract information from the ventricular electrogram (EGM) recorded by implantable cardioverter defibrillators (ICD) aside from the discrimination of supraventricular tachycardia and ventricular tachycardia. The current study aims to examine the effect of ischemia in the major coronary artery distributions on the shock EGM from ICDs.
Methods: Domestic crossbred pigs (n = 10, 20–40 kg) were implanted with a dual-coil right ventricular defibrillation system. Through the femoral approach, percutaneous balloon occlusion of the major coronary arteries was performed. The left anterior descending (LAD), left circumflex (LCx), and right coronary (RCA) arteries were occluded in random order for 3–5 minutes with 30-minute periods of reperfusion in between and the shock EGMs were recorded and analyzed.
Results: During peak ischemia, R wave amplitude increased by a mean of 204.3% (P = 0.003), increased by a mean of 73.8% (P = 0.0009), and decreased by a mean of 28.0% (P = 0.109) in the LAD, LCx, and RCA territories, respectively. During peak ischemia ST segments elevated by a mean of 105.3% (P = 0.041), elevated by a mean of 114.9% (P = 0.064), and decreased by a mean of 584.5% (P = 0.006) in the LAD, LCx, and RCA territories, respectively.
Conclusions: Ischemia affects ICD shock EGMs in a manner that appears to vary depending on the culprit vessel. Our data demonstrate the feasibility of ischemia detection from ICD shock EGMs.     

The prevalence, incidence and prognostic value of the Brugada-type electrocardiogram: a population-based study of four decades

OBJECTIVES: We sought to demonstrate the prevalence, incidence and prognostic value of the Brugada-type electrocardiogram (ECG) in a general population. BACKGROUND: The Brugada syndrome is characterized by evidence of right bundle branch block and ST segment elevation in the right precordial leads, as well as sudden death caused by ventricular fibrillation. However, the natural history of the Brugada-type ECG remains unclear. METHODS: We investigated 4,788 subjects (1,956 men and 2,832 women) who were <50 years old in 1958 and had undergone biennial health examinations, including electrocardiography, through 1999. The Brugada-type ECG was defined as a terminal r' wave in lead V(1) and ST segment elevation > or =0.1 mV in leads V(1) and V(2). Unexpected death was defined as sudden death or unexplained accidental death. RESULTS: There were a total of 32 Brugada-type ECG cases; the prevalence and incidence were 146.2 in 100,000 persons and 14.2 persons per 100,000 person-years, respectively. The incidence was nine times higher among men than women, and the average age at presentation was 45 +/- 10.5 years. The Brugada-type ECG appeared intermittently in most cases and was found in 26% of subjects who died unexpectedly. Cox survival analysis revealed that mortality from unexpected death was significantly higher in subjects with a Brugada-type ECG than in control subjects (p < 0.01). Unexpected deaths were more frequent among subjects with the Brugada-type ECG who had a history of syncope (p < 0.05). CONCLUSIONS: The Brugada-type ECG is not a very rare condition in the adult Japanese population. Subjects with a Brugada-type ECG have an increased risk of unexpected death.     

Prognostic significance of ST segment depression in lateral leads I, aVL, V5 and V6 on the admission electrocardiogram in patients with a first acute myocardial infarction without ST segment elevation

OBJECTIVES

We sought to investigate the short-term prognostic value of the admission electrocardiogram (ECG) in patients with a first acute myocardial infarction (MI) without ST segment elevation.

BACKGROUND

ST segment depression on hospital admission predicts a worse outcome in patients with a first acute MI, but the prognostic information provided by the location of ST segment depression remains unclear.

METHODS

In 432 patients with a first acute MI without Q waves or ≥0.1 mV of ST segment elevation, we evaluated the ability of the initial ECG to predict in-hospital death.

RESULTS

The presence, magnitude and extent of ST segment depression were associated with an increased mortality, but the only electrocardiographic variable that was significant in predicting death after adjusting for baseline predictors was ST segment depression in two or more lateral (I, aVL, V₅, or V₆) leads (odds ratio 3.5, 95% confidence interval 1.2 to 10.6). Patients with lateral ST segment depression (n = 91, 21%) had higher rates of death (14.3% vs. 2.6%, p < 0.001), severe heart failure (14.3% vs. 4.1%, p < 0.001) and angina with electrocardiographic changes (20.0% vs. 11.6%, p = 0.04) than did the remaining patients, even though they had similar peak creatine kinase, MB fraction levels (129 ± 96 vs. 122 ± 92 IU/liter, p = NS). In contrast, ST segment depression not involving the lateral leads did not predict a poor outcome. Among patients who were catheterized, those with lateral ST segment depression had a lower left ventricular ejection fraction (57 ± 12% vs. 66 ± 13%, p = 0.001) and more frequent left main coronary artery or three-vessel disease than did the remaining patients (60% vs. 22%, p < 0.001).

CONCLUSIONS

In patients with a first non–ST segment elevation acute MI, ST segment depression in the lateral leads on hospital admission predicts a poor in-hospital outcome.     

头胸导联右胸心电图诊断急性右室梗塞的价值

选择急性下壁合并右室梗塞（依据血液动力学诊断）患者３４例，比较其同部位、同时间右胸Ｗｉｌｓｏｎ导联（Ｖ３Ｒ～Ｖ７Ｒ）和头胸导联（ＨＶ３Ｒ～ＨＶ７Ｒ）的心电图，探讨后者诊断急性右室梗塞的价值。首次记录心电图的时间为发病１０（平均４±２．８）ｈ２４例（Ａ组），超过１０（平均３１±１６．８）ｈ１０例（Ｂ组），两组Ｖ５Ｒ～Ｖ７Ｒ、ＨＶ５Ｒ～ＨＶ７Ｒ导联病理性Ｑ波出现率均为１００％。Ｖ４Ｒ（ＨＶ４Ｒ）或Ｖ７Ｒ（ＨＶ７Ｒ）ＳＴ段抬高≥０．１ｍＶ者，Ａ组为１００％，Ｂ组Ｗｉｌｓｏｎ导联为６０％、头胸导联为１００％。头胸导联ＳＴ段抬高幅度高于Ｗｉｌｓｏｎ导联０．０５～０．１５ｍＶ；头胸导联不仅ＱＲＳ－Ｔ波群呈现急性损伤期向充分发展期的衍变与ａＶＦ导联一致，并且ＳＴ段抬高持续的时间也与ａＶＦ导联一致，此特征有利于急性右室梗塞的诊断。     

Prognostic significance of ST segment depression in lateral leads I, aVL, V5 and V6 on the admission electrocardiogram in patients with a first acute myocardial infarction without ST segment elevation

OBJECTIVESWe sought to investigate the short-term prognostic value of the admission electrocardiogram (ECG) in patients with a first acute myocardial infarction (MI) without ST segment elevation.BACKGROUNDST segment depression on hospital admission predicts a worse outcome in patients with a first acute MI, but the prognostic information provided by the location of ST segment depression remains unclear.METHODSIn 432 patients with a first acute MI without Q waves or ≥0.1 mV of ST segment elevation, we evaluated the ability of the initial ECG to predict in-hospital death.RESULTSThe presence, magnitude and extent of ST segment depression were associated with an increased mortality, but the only electrocardiographic variable that was significant in predicting death after adjusting for baseline predictors was ST segment depression in two or more lateral (I, aVL, V₅, or V₆) leads (odds ratio 3.5, 95% confidence interval 1.2 to 10.6). Patients with lateral ST segment depression (n = 91, 21%) had higher rates of death (14.3% vs. 2.6%, p < 0.001), severe heart failure (14.3% vs. 4.1%, p < 0.001) and angina with electrocardiographic changes (20.0% vs. 11.6%, p = 0.04) than did the remaining patients, even though they had similar peak creatine kinase, MB fraction levels (129 ± 96 vs. 122 ± 92 IU/liter, p = NS). In contrast, ST segment depression not involving the lateral leads did not predict a poor outcome. Among patients who were catheterized, those with lateral ST segment depression had a lower left ventricular ejection fraction (57 ± 12% vs. 66 ± 13%, p = 0.001) and more frequent left main coronary artery or three-vessel disease than did the remaining patients (60% vs. 22%, p < 0.001).CONCLUSIONSIn patients with a first non–ST segment elevation acute MI, ST segment depression in the lateral leads on hospital admission predicts a poor in-hospital outcome.     

Arrhythmogenic right ventricular dysplasia--ARVD--case study

A case of 20-year-old male with arrhythmogenic right ventricular dysplasia (ARVD) is presented. The patient was admitted to hospital due to exercise-related syncope which was preceded by palpitations. ECG, echocardiography, radionuclide ventriculography and endomyocardial biopsy confirmed the diagnosis of ARVD. Coronary angiography was normal. Exercise testing revealed ST segment elevation in the right precordial leads at the peak exercise, followed by sustained ventricular tachycardia of the left bundle branch block morphology, terminated by intravenous lignocaine. The patient received pacemaker and sotalol. During five-year follow-up no recurrences of syncope were observed and repeated Holter ECG monitoring demonstrated marked reduction of spontaneous ventricular ectopy.