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SUMMARY The relationship of changes in ventricular activation patterns and variations in R-wave amplitude on the surface ECG during the hyperacute phase of myocardial ischemia were studied in nine open-chest dogs. The sum of R-wave amplitude (2RWA) changes in surface ECG leads L2, V5 and Frank orthogonal leads X, Y and Z were correlated with changes in the conduction time along the specialized conduction.system and in intramyocardial conduction times, as well as with hemodynamic and echocardiographically determined left ventricular dimensional changes. The hyperacute phase of myocardial ischemia induced by a one-stage occlusion of the left circumflex coronary artery was marked by a progressive increase in left ventricular enddiastolic diameter and left ventricular end-diastolic pressure as well as a progressive decrease in cardiac output. At the same time, ZRWA and intramyocardial conduction time followed a synchronous biphasic pattern. In the first 30 seconds after coronary artery ligation, intramyocardial conduction time in the ischemic zone accelerated to a peak of 11.3% above control (p < 0.001). This acceleration of conduction was followed closely by a decrease in ZRWA to 16.8% below control (p < 0.001). A second phase ensued, characterized by a gradual slowing of intramyocardial conduction time in the ischemic zone to 135.1% above control (p < 0.001) and a synchronous increase in 2RWA to 53.1% above control (p < 0.001). Conduction time along the specialized conduction system did not change significantly.Thus, the asynchrony of ischemic 2RWA alterations with hemodynamic and left ventricular dimensional changes and the similarity of the biphasic responses of 2RWA to the changes in intramyocardial conduction time in the ischemic area suggest that ventricular activation patterns rather than hemodynamic and intracardiac dimensional changes may play the major role in determining R-wave amplitude responses to acute myocardial ischemia.INCREASED R-wave amplitude on the surface ECG at peak exercise has been observed frequently in patients with coronary artery disease. 1-4 Bonoris et al.1 claimed this sign to be a sensitive and specific marker for the diagnosis of coronary artery disease. Increases in R-wave amplitude may also indicate the extent of ischemia-induced left ventricular dysfunction.2 4 This suggestion is based on the assumption that R-wave amplitude changes are related, by the Brody effect,5 to an increase in left ventricular volume resulting from acute ischemia. However, studies in humans have not consistently corroborated these findings."8We designed a series of experiments using a canine model of acute myocardial ischemia to identify factors that contribute to ischemic R-wave amplitude alterations. In our initial studies we showed that ischemic Rwave amplitude changes could not be explained merely by intracardiac volume changes.9' 10 Other in- From vestigators have shown that ventricular activation patterns influence the R-wave amplitude response to volume changes in the normal heart."-"' The purpo...

Background: Pulmonary function and patient complaints appear to improve up to 12 months after lobectomy but long-term prospective studies based on clinical data are scarce. Improvement in pulmonary function may depend on the area and extent of the resection and the time from the operation. This prospective study aimed to determine pulmonary function changes according to the resected lobe. Methods: This prospective study included 59 patients requiring single lobectomy. Total volume and lowattenuation volume (LAV) for each lobe and the entire lungs were calculated based on helical computed tomography images. Vital capacity (VC), forced expiratory volume in one second (FEV 1 ), percent FEV 1 (%FEV 1 ), percent lung diffusion capacity for carbon monoxide (%DL co ), %DL co divided by the alveolar volume (%DL co /V A ), modified Medical Research Council (mMRC) grades, and COPD Assessment Test (CAT) scores were compared at 3, 6, and 12 months after surgery. Results: VC was higher at 12 months than at 3 months after right upper lobectomy (RUL) or right lower lobectomy (RLL). FEV 1 and %FEV 1 were higher at 12 months than at 6 months after left lower lobectomy (LLL). %DL co was higher at 12 months than at 3 months after RUL or left upper lobectomy (LUL). DL co / V A , mMRC grades, and CAT scores did not change significantly in the period from 3 to 12 months after any lobectomy procedure. Compared to the predicted postoperative values, the observed values of VC for RUL, RLL, and LUL; FEV 1 for RLL; %FEV 1 for RLL and LUL; %DL co for LUL; and %DL co /V A for all lobectomy procedures were higher at 12 months. Conclusions: Improvements in pulmonary function and symptoms varied according to the resected lobe. Some of the observed pulmonary function values were higher than the predicted postoperative values.Pulmonary function changes may be related to the location, volume, and extent of emphysematous changes.

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SUMMARY Diastolic mitral valve "locking," defined as sustained diastolic closure of the mitral valve after atrial systole, was investigated by simultaneous hemodynamic and echocardiographic recordings during a protocol of programmed pacing in six dogs with surgically induced atrioventricular block. Atrial extrasystoles were introduced at progressively increasing coupling intervals during programmed prolonged pauses in ventricular pacing. As the coupling interval of the atrial extrasystole was increased, both the mitral reopening time (MRT) and the calculated left ventricular volume (LVV) at the end of the MRT increased proportionally. These interrelations could be best expressed by a general logarithmic function of the form y = a + b In (x), where x = the coupling interval of the atrial extrasystole and y = the MRTor the LVV. Correlations between the measured data and the predicted data were excellent (r ¢ 0.95). In each dog, a specific LVV had to be attained to allow a diastolic "locking" of the mitral valve. Atrial standstill and atrial fibrillation were also induced in each dog to study the relative role of atrial systole in locking of the mitral valve. During either atrial standstill or atrial fibrillation, the mitral valve closed transiently, but did not lock, despite the accumulation of a LVV larger than the LVV necessary to lock the valve during sinus rhythm. Thus, diastolic locking of the mitral valve has several determinants, including the presence of active atrial systole and the accumulation of a sufficient intraventricular volume.THE MECHANISMS of mitral valve closure have been studied, but not completely elucidated. In 1843, Baumgarten' postulated that atrial contraction was an important element in the presystolic closure of the mitral leaflets. Others have shown that the abrupt cessation of rapid forward flow through the mitral valve at the end of atrial systole and the vortex formation or eddy currents behind the mitral leaflets may be important in the initiation of mitral valve closure.`4 Evidence for these hypotheses has been obtained in both experimental and human studies.2-19 However, Dean6 observed that in the absence of a subsequent, properly timed ventricular systole, the mitral valve, previously closed by atrial systole, tended to reopen and assume a "midstream" position. It was apparent, therefore, that the contribution of atrial systole to mitral valve motion could only initiate a closing motion of the mitral valve, but was insufficient to "lock" the valve in the closed position for the duration of diastole. The mechanisms that sustain diastolic mitral valve "locking" have never been demonstrated. In this study, we correlated echocardiographic and hemodynamic data obtained during various patterns of atrioventricular (AV) pacing in an experimental canine model. Material and MethodsThe study was performed in six healthy mongrel