Plaque rupture is associated with morphologic characteristics of vulnerable lesions, as well as with larger infarcts and a higher incidence of no-reflow phenomenon, suggesting that plaque embolism contributes to the progression of myocardial damage in patients with anterior AMI.

Diastolic mitral regurgitation (MR) may be induced by prolonging atrioventricular (AV) delay, and a significant negative correlation has been described between the critical PQ interval for the appearance of diastolic MR and pulmonary capillary wedge pressure (PCWP) in patients with DDD pacemakers. We report the relationship between the critical PQ interval for the appearance of diastolic MR and the optimal PQ interval in 11 patients (69.1 +/- 12.6 years). Cardiac output (CO) and PCWP were measured by Swan-Ganz catheter and transmitral blood flow was recorded by pulsed-Doppler echocardiography. AV delay was prolonged stepwise by 0.025 seconds starting from 0.065 seconds. The pacing rate was fixed at 70 beats/min. CO was highest when the PQ interval was 0.18 +/- 0.04 seconds. There was a significant positive correlation between the critical PQ interval for the appearance of diastolic MR and the PQ interval at which CO was the highest (r = 0.91, P < 0.01). The PQ interval at which CO was the highest was 0.02 +/- 0.02 seconds shorter than the critical PQ interval for the appearance of diastolic MR (P < 0.05). When the PQ interval was increased by 0.025 seconds from the critical PQ interval for the appearance of diastolic MR, CO decreased from 4.3 +/- 0.6 L/min to 4.1 +/- 0.6 L/min and PCWP increased from 7.5 +/- 6.4 mmHg to 8.5 +/- 7.3 mmHg (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

he efficacy of a short atrioventricular (AV) delay in patients with severely impaired cardiac function has been reported, 1-3 but the delay required to achieve optimal AV synchrony varies from patient to patient and may change with changes in cardiac function.Diastolic mitral regurgitation (MR) is observed in patients with elevated left ventricular end-diastolic pressure 4 and can be induced by prolonging the AV delay in patients with DDD pacemakers. [5][6][7][8][9][10][11][12] Cardiac function may be improved by AV sequential pacing and by setting the AV delay at less than the critical PQ interval for the appearance of diastolic MR when the latter is observed in patients with intrinsic AV conduction. 11 We have determined a new formula for predicting the optimal AV delay using Doppler echocardiography: optimal AV delay = slightly prolonged AV delay -interval between the end of the atrial kick and complete closure of the mitral valve (duration of diastolic MR) at the AV delay setting (Fig 1). 12 We report a patient with severe congestive heart failure who remained in good condition for more than 4 years with pacemaker implantation and AV delay optimization. Case ReportThe patient, an 84-year-old man with an old myocardial infarction, had had percutaneous transluminal angioplasty for total occlusion of the proximal portion of the left ascending artery successfully performed in August 1994. Although there had not been restenosis or progression of the coronary artery lesion, he had repeated admissions to hospital for congestive heart failure (Fig 2A). Medications were unchanged during follow-up (oral administration of furosemide 40 mg, spironoractone 25 mg, digoxine 0.125 mg, captopril 18.75 mg, isosorbide dinitrate 60 mg, nicorandil 15 mg, aspirin 100 mg daily). He complained of dizziness, but the dose of captopril could not be increased andblocker could not be used because of the risk of hypotension or bradycardia.ECG showed prolongation of the PQ interval (0.28 s) and complete left bundle branch block (Fig 2B). The Hisventricular interval was prolonged (90 ms on intracardiac electrocardiogram) and the ejection fraction was 31%, estimated by left ventriculography. Marked diastolic MR was detected ( Fig 3A) and during 80 beats/min AV sequential pacing, it was observed when the AV delay was set at 240 ms. The interval between the end of the atrial kick and complete closure of the mitral valve (duration of diastolic MR) was 120 ms (Fig 3B). Therefore, by our method, the predicted optimal AV delay was 240 -120 = 120 ms, and the diastolic MR disappeared when the AV delay was set at 120 ms (Fig 3C). Cardiac output was 4.7 L/min during 80 /min Tomohiko Shigemasa, MD; Tsutomu Endo, MD; Kazuo Kimura, MD; Takashi Usui, MD; Satoshi Umemura, MD 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)...

Background: Recent pacemakers with transthoracic impedance sensors have a specific algorithm identifying sleep apnea (SA). Our aim was to evaluate the algorithm in Japanese patients. Methods: Consecutive patients implanted with a pacemaker with sleep apnea monitoring algorithm at our hospital were enrolled prospectively. After implantation, patients underwent polysomnography (PSG). The respiratory disturbance index measured by pacemaker (RDI-PM) was extracted in the morning after PSG. Results: Forty-five patients were recruited; 78% of patients underwent overnight PSG completely, and among them RDI-PM was invalid for one patient. Then the analysis was performed in 34 patients. Moderate/severe SA (apnea hypopnea index, AHI ! [ 5 5 _ T D $ D I F F ] 15 events/h) and severe SA (AHI ! [ 5 6 _ T D $ D I F F ] 30 events/h) by PSG were diagnosed in 65% and 41% of patients. The mean AHI-PSG and RDI-PM were 30.4 AE 22.6 and 21.7 AE 14.2 events/h, respectively. There was a significant positive correlation between AHI-PSG and RDI-PM ([ 8 _ T D $ D I F F ] r = 0.543; p = 0.001). The correlation was stronger in the severe SA group ([ 8 _ T D $ D I F F ] r = 0.664; p = 0.010), in a group whose apnea index was higher than hypopnea index ([ 8 _ T D $ D I F F ] r = 0.822; p = 0.002), and in a group whose central sleep apnea (CSA) index was higher than obstructive sleep apnea index ([ 8 _ T D $ D I F F ] r = 0.977; p < 0.001). RDI-PM cut-off value for identifying severe SA was 22 (area under the curve, 0.682; sensitivity, 64%; specificity, 75%). Conclusions: The pacemaker-based algorithm is a useful screening tool for SA in Japanese individuals, especially in the severe SA group, apnea-dominant group, and CSA-dominant group.

The aim of this study was to assess the association between the spatial location of plaque rupture and remodeling pattern of culprit lesions in acute anterior myocardial infarction (MI). Positive remodeling suggests a potential surrogate marker of plaque vulnerability, whereas plaque rupture causes thrombus formation followed by coronary occlusion and MI. Intravascular ultrasound (IVUS) can determine the precise spatial orientation of coronary plaque formation. We studied 52 consecutive patients with acute anterior MI caused by plaque rupture of the culprit lesion as assessed by preintervention IVUS. The plaques were divided into those with and without positive remodeling. We divided the plaques into three categories according to the spatial orientation of plaque rupture site: myocardial (inner curve), epicardial (outer curve), and lateral quadrants (2 intermediate quadrants). Among 52 plaque ruptures in 52 lesions, 27 ruptures were oriented toward the epicardial side (52%), 18 toward the myocardial side (35%), and 7 in the 2 lateral quadrants (13%). Among 35 plaques with positive remodeling, plaque rupture was observed in 21 (52%) on the epicardial side, 12 (34%) on the myocardial side, and 2 (6%) on the lateral side. However, among 17 plaques without positive remodeling, plaque rupture was observed in 6 (35%), 6 (35%), and 5 (30%), respectively (p = 0.047). Atherosclerotic plaques with positive remodeling showed more frequent plaque rupture on the epicardial side of the coronary vessel wall in anterior MI than those without positive remodeling.