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BACKGROUND: Patients with an anterolateral acute myocardial infarction (AMI) have a worse prognosis, and those with additional inferolateral wall involvement might be higher risk because of more extensive area at risk. Lead -aVR obtained by inversion of images in lead aVR has been reported to provide useful information for inferolateral lesion. METHODS: We examined the relation between ST-segment deviation in lead aVR on admission electrocardiogram (ECG) and left ventricular function in 105 patients with an anterolateral AMI undergoing successful reperfusion < or = 6 hours after onset. Patients were classified according to ST-segment deviation in lead aVR on admission ECG: group A, 23 patients with ST elevation of > or = 0.5 mm; group B, 47 patients without ST deviation; and group C, 35 patients with ST depression of > or = 0.5 mm. RESULTS: There were no differences among the 3 groups in age, sex, or site of the culprit lesion. In groups A, B, and C, the peak creatine kinase level was 3661 +/- 1428, 4440 +/- 1889, and 6959 +/- 2712 mU/mL, and the left ventricular ejection fraction (LVEF) measured by predischarge left ventriculography was 54% +/- 9%, 48% +/- 7%, and 37% +/- 9%, respectively(P < .01). During hospitalization, congestive heart failure occurred more frequently in group C than in groups A or B (P < .05). ST-segment depression in lead aVR had a higher predictive accuracy than other ECG findings in identifying patients with predischarge LVEF < or = 35%. CONCLUSIONS: We conclude that in patients with an anterolateral AMI, ST-segment depression in lead aVR on admission ECG is useful for predicting larger infarct and left ventricular dysfunction despite successful reperfusion.

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BACKGROUND: ST-segment elevation of > or = 1.0 mm in lead V4R has been shown to be a reliable marker of right ventricular involvement (RVI), a strong predictor of a poor outcome in patients with inferior acute myocardial infarction (IMI). However, patients with no ST-segment elevation in lead V4R despite the presence of RVI have received little attention. HYPOTHESIS: The study was undertaken to study the clinical features of patients with no ST-segment elevation in lead V4R despite the presence of RVI, which means false negative, as such patients have received little attention in the past. METHODS: We studied 62 patients with a first IMI, who had total occlusion of the right coronary artery (RCA) proximal to the first right ventricular branch and successful reperfusion within 6 h from symptom onset, to examine the implications of the absence of ST-segment elevation in lead V4R despite the presence of RVI. RESULTS: A standard 12-lead electrocardiogram (ECG) and right precordial ECG (lead V4R) were recorded on admission, and three posterior chest ECGs (leads V7 to V9) were additionally recorded in 34 patients. Patients were classified according to the absence (Group 1, n = 18) or presence (Group 2, n = 44) of ST-segment elevation of > or = 1.0 mm in lead V4R on admission. Patients in Group 1 had a greater ST-segment elevation in leads V7 to V9 (2.9+/-2.4 vs. 1.4+/-3.0 mm. p < 0.05), a higher frequency of a dominant RCA (defined as the distribution score > or = 0.7) (72 vs. 11%, p < 0.001), and a higher peak creatine kinase level (3760+/-1548 vs. 2809+/-1824 mU/ml, p < 0.05) than those in Group 2. CONCLUSIONS: In patients with IMI caused by the occlusion of the RCA proximal to the first right ventricular branch, no ST-segment elevation in lead V4R can occur because of concomitant posterior involvement. In such patients, the incidence of RVI may be underestimated on the basis of ST-segment elevation in lead V4R.

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BACKGROUND: Patients with occlusion of the left anterior descending coronary artery (LAD) proximal to both the first septal branch and the first diagonal branch may benefit most from early reperfusion therapy due to extensive area at risk. HYPOTHESIS: The aim of the study was to examine whether 12-lead electrocardiograms (ECGs) in the acute phase of acute myocardial infarction (AMI) could identify total occlusion of the LAD proximal to both the first septal and the first diagonal branch. METHODS: A 12-lead electrocardiogram was recorded on admission in 128 patients with anterior AMI within 12 h from symptom onset. Patients were divided into three groups according to the culprit lesion: 33 patients had total occlusion of the LAD proximal to both the first septal perforator and the first diagonal branch (Group P), in 51 it was proximal to either the first septal perforator or the first diagonal branch (Group D-a), and in 44 it was distal to both the first septal perforator and the first diagonal branch (Group D-b). RESULTS: Sensitivity and specificity of a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL were 85 and 95%, respectively, which was better than the results derived by all other ECG criteria (p< 0.001). CONCLUSIONS: We conclude that a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL is a useful predictor of proximal LAD occlusion in patients with anterior AMI.

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It has been reported that cardiac function can be improved by implanting a DDD pacemaker (PM) and setting a short atrioventricular (AV) delay in patients with impaired cardiac function. A previous report found that the critical AV delay that induces diastolic mitral regurgitation (MR) may represent the upper limit of the optimal AV delay. The optimal AV delay can be predicted by a simple method: slightly prolonged AV delay minus the interval between the end of the atrial kick and complete closure of the mitral valve (duration of diastolic MR) at the AV delay setting. The patient was a 84-year-old man with an old myocardial infarction. He had repeated admissions to hospital for congestive heart failure. ECG showed prolongation of the PQ interval (0.28 s) and complete left bundle branch block. Cardiac function was improved by AV sequential pacing when the AV delay was set at 120ms. After DDD-PM implantation, the cardiothoracic ratio decreased from 57 to 45% and cardiac function was improved from New York Heart Association class III to I. The AV delay was optimized during follow-up. Four years after PM implantation, the patient was in good condition without further hospital admission.

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The cardiovascular and sympatholytic effects of combination therapy with guanabenz were examined in 26 patients (48 +/- 13 years old [mean +/- SD]) with stage 2 and 3 hypertension. Included in the study were patients under treatment with conventional antihypertensive drugs whose systolic and diastolic blood pressure was above 140 and 90 mmHg, respectively. Blood pressure, heart rate, and sympathetic parameters such as plasma concentration of norepinephrine and muscle sympathetic nerve activity at rest as well as during ambulatory conditions, 24-hour urinary excretion of norepinephrine, and low frequency (LF: 0.04-0.15 Hz)/high frequency (HF: 0.15-0.4 Hz) power ratio as a marker of cardiac sympathetic activity during 24 hours were examined before and after guanabenz (4-8 mg/d) combination therapy with first-line antihypertensive drugs such as diuretics. Left ventricular mass index (LVMI) was also calculated by conventional echocardiography. After 32 weeks of guanabenz combination therapy, systolic and diastolic blood pressure, heart rate, plasma and urinary excretion of norepinephrine, muscle sympathetic nerve activity, and LF/HF power ratio were significantly decreased, while neither LF nor HF power was changed. LVMI was also significantly decreased (270 +/- 81 vs. 236 +/- 83 g/m2, p < 0.005). These results indicate that guanabenz combination therapy inhibits sympathetic nerve activity under resting conditions as well as during ambulatory conditions and may accelerate regression of left ventricular hypertrophy in patients with moderate to severe hypertension.

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1. The role of angiotensin (Ang)II in and the effects of angiotensin-converting enzyme (ACE) inhibitors on the regulation of sympathetic neural activity were examined in humans. 2. We measured baseline values of muscle sympathetic nerve activity (MSNA) and its reflex inhibition in 28 patients with essential hypertension with elevated plasma renin activity (PRA; > 1.0 ng/mL per h = 0.28 ng/L per s) before and after either acute or chronic oral administration of an ACE inhibitor or placebo and in 20 normotensive subjects before and after infusion of either AngII (5 ng/kg per min = 4.8 pmol/kg per min) or vehicle (5% dextrose). Muscle sympathetic nerve activity was recorded from the tibial nerve and its reflex inhibition was evaluated during pressor responses to bolus injection of phenylephrine (2 micrograms/kg, i.v.). 3. Blood pressure was significantly decreased (P < 0.01) after the acute oral administration of captopril (25 mg), accompanied by a slight increase in MSNA in patients with essential hypertension compared with control patients who received placebo administration. Reflex changes in MSNA were significantly augmented after oral administration of captopril (-4.1 +/- 0.5 vs -6.2 +/- 0.6%/mmHg, respectively; P < 0.01), with a significant reduction of plasma AngII, while they were not affected by placebo administration. 4. In contrast, acute AngII infusion was accompanied by decreases in both PRA and MSNA in normotensive subjects. Reflex changes in MSNA were significantly reduced after AngII infusion (-11.0 +/- 0.8 vs -7.4 +/- 1.0%/mmHg, respectively; P < 0.01) but not after vehicle alone. 5. Chronic ACE inhibition by 12 week oral imidapril administration (5-10 mg/day) significantly (P < 0.05) decreased baseline values of MSNA, which were accompanied by a significant (P < 0.05) increase in the reflex inhibition of MSNA, while plasma concentrations of noradrenaline were unaffected. 6. These results indicate that AngII blunts reflex inhibition of sympathetic neural activity and that inhibition of the renin-angiotensin system by an ACE inhibitor augments reflex regulation of sympathetic neural activity and reduces baseline values in patients with essential hypertension.

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Because adipose tissue has high electric resistance, the amount of body fat influences ECG voltage. In this study, body fat weight of patients with essential hypertension was measured by means of the impedance method and was used to correct mean ECG voltage. Then the relation between body fat-corrected mean ECG voltage (Vfm) and ambulatory blood pressure (BP) was investigated. The subjects were 172 patients with essential hypertension (88 men, 84 women, none receiving medication) between the ages of 30 and 75 years. Ambulatory BP was measured by a multi-biomedical recorder. Minimum sleep-time BP (base BP) was calculated to correspond with minimum sleep-time heart rate. The tetrapolar bioelectric impedance method was used to measure body fat (kg). Left ventricular mass (LVM) was obtained by echocardiography. Then comparisons were made with standard 12-lead ECG, and the statistical mean ECG voltage (Vm) and Vfm were derived by multivariate statistical analysis. The following formula was devised to obtain Vfm resulting from the multivariate analysis that demonstrated a high correlation with LVM (r=0.85): Vfm=0.175(Body Fat)1/3xVm+0.5 (mV). The coefficient of correlation (r) between Vfm and ambulatory BP was not smaller than that between LVM and ambulatory BP. Base systolic BP demonstrated a significantly higher r value (r=0.83) with Vfm/BSA1/2 (where BSA is body surface area) than mean daytime SBP (r=0.65). In many subjects with white-coat hypertension, Vfm/BSA1/2 was <1.33 mV/m (34 of 38 cases; sensitivity, 89%; specificity, 89%). These results indicate that Vfm is a better indicator of hypertensive left ventricular hypertrophy and that it may be useful in estimating minimum sleep-time systolic BP and in diagnosing white-coat hypertension in the outpatient clinic.

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QT interval may change when cardiac function is improved by optimizing the atrioventricular the (AV) delay. The relationship between AV delay, QT interval and cardiac function in patients with implanted DDD pacemakers was studied in 12 patients (aged 71+/-12 SD years) with complete or high degree AV block. Cardiac output (CO) was measured using a Swan-Ganz catheter or by continuous Doppler echocardiography. The pacing rate was fixed at 70-80/min to eliminate the influence of heart rate. The AV delay was prolonged stepwise by 30 ms starting from 90 ms. All measurements were performed after 5 min of pacing. When the AV delay was prolonged, the CO and QT interval gradually increased and reached a peak, and then decreased. When the CO was increased from the minimum to the maximum value by optimizing the AV delay, the QT interval was significantly prolonged from 440+/-40 to 456+/-39 ms (P<0.002). The CO increased from 5.5+/-2.5 to 6.0+/-2.5 l x min(-1) (P<0.002) when the AV delay was changed, during which the QT interval was prolonged from the minimum to the maximum value. There was a significant positive correlation between the optimal AV delay at which CO was maximal (161+/-33 ms) and the optimal AV delay predicted from the maximum QT interval (167+/-29 ms, r=0.85, P<0.001). In conclusion, the optimal AV delay can be predicted from the QT interval.

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The effects of right ventricular outflow pacing were studied in 13 patients (mean [+/-SD] 69.8 +/- 8.2 years old). All patients received DDD pacemakers except two patients with implanted VVI pacemakers who had chronic atrial fibrillation. Cardiac output and pulmonary capillary wedge pressure were measured by Swan-Ganz catheter. Pacing rate was fixed at 70-80/min and atrioventricular delay was fixed at 165 msec. When the pacing site was changed from the right ventricular apex to the right ventricular outflow during right ventricular pacing in 11 patients, cardiac output increased from 3.3 +/- 0.6 to 3.4 +/- 0.5 l/min (p < 0.001), and wedge pressure decreased from 9.3 +/- 1.9 to 8.8 +/- 2.0 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow during atrioventricular pacing in eight patients, cardiac output increased from 3.9 +/- 0.4 to 4.0 +/- 0.4 l/min (p < 0.05), and wedge pressure decreased from 7.1 +/- 2.3 to 6.6 +/- 2.1 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow in seven patients with ejection fraction (EF) greater than 55%, cardiac output increased from 3.6 +/- 0.5 to 3.7 +/- 0.4 l/min (p < 0.05), and in four patients with EF less than 55%, it increased from 2.9 +/- 0.4 to 3.0 +/- 0.4 l/min (p < 0.01). Cardiac function was improved by right ventricular outflow pacing compared to right ventricular apex pacing regardless of the pacing mode or cardiac function.

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Angiotensin-converting enzyme (ACE) inhibitors now have an accepted place in the treatment of hypertension and congestive heart failure. With the discovery and development of captopril, several other ACE inhibitors have been synthesized and introduced for clinical use. All ACE inhibitors bind to zinc ions located in the active site of the ACE molecule. ACE inhibitors can be classified according to the ligand of the zinc ion of ACE, into 3 different structural types: (1) the first type such as captopril has a sulphhydryl moiety as the ligand; (2) the second type such as enalapril uses a carboxyl moiety as the ligand; (3) the third type such as fosinopril uses neither a sulphhydryl nor carboxyl group, but a phosphinic acid as the zinc binding moiety. ACE inhibitors can also be classified according to the excretion route of their active moiety, into 2 different excretion route types:(1) excreated mainly through the kidney such as captopril, enalaprilat, lisinopril, benazeprilat, imdaprilat, trandraprilat, etc.; (2) excreated both in the bile and urine such as fosinoprilat, temocaprilat, zofenoprilat etc. ACE inhibitors have clinically beneficial effects not only for patients with either hypertension or congestive heart failure, but also can be used to prevent the progression of renal dysfunction induced by hypertension and diabetes mellitus.

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