Autopsy studies of hearts from 140 patients who had suffered acute myocardial infarction (AMI) and 26 cases of sudden coronary death revealed two distinct types of myocardial cell death: "kinetic cell death" (KD) and "static cell death" (SD). In KD, the predominant type of cell death in AMI-myofibrils disintegrated through alternating overcontraction and overextension. KD was found not only in patients having died after some time had elapsed from the onset of AMI, but also in cases of sudden coronary death. Muscle fibers in SD, which by contrast began to appear at least seven hours after the onset of AMI, characteristically preserved cross striations, while their nuclei were pyknotic or had already disappeared. Such fibers were observed only in territories peripheral to occlusive coronary thrombus, a secondary rather than a primary event that takes place during the course of AMI. As a result of the above observations, we were able to produce a new experimental model of AMI using mongrel dogs. As a preparatory procedure we first injected them intravenously with 2% calcium chloride at a constant rate for 90 or 120 minutes, and then with a sudden injection of caffeine, calcium chloride and catecholamine in order to induce KD. In contrast, ligation of the intraventricular coronary artery near its origin caused SD of myocardial fibers in the dependent territories. Overall results led us to conclude that AMI is initiated by instantaneous overcontraction of myocardial fibers, resulting in their KD, a phenomenon that could be called "myocardial self-destruction." 相似文献
High-power short-duration (HP-SD) ablation could reduce collateral tissue damage by shortening the conductive heating phase. However, it is difficult to evaluate the transmural effect of ablation lesions during pulmonary vein isolation (PVI) procedures. The present study aimed to evaluate the change in superior vena cava (SVC) potential delay as a surrogate marker of collateral tissue damage during right PVI, which is adjacent to SVC.
Methods
Out of 250 consecutive patients who underwent PVI, 86 patients in whom SVC potential during sinus rhythm was recorded both before and after right PVI were analyzed. In 46 of the patients, an HP-SD setting of 45–50 W was used (HP-SD group). In the remaining 40 patients, a conventional power setting of 20–30 W was used (conventional group). We compared the change in SVC potential delay after right PVI, radiofrequency energy, and mean contact force in the anterior–superior right PVI line, which was close to the posterior aspect of SVC, between the two groups.
Results
Although the total delivered radiofrequency energy (2,924 J vs. 2,604 J) and the mean contact force (18.5 g vs. 16.0 g) in the SVC overlapping area did not differ, the change in SVC potential delay after right PVI was significantly longer in the conventional group compared to the HP-SD group (5.0 ms vs. 0.0 ms, p?<?0.001).
Conclusions
The changes in SVC potential delay after right PVI might be a surrogate marker of collateral tissue damage according to the used energy settings.
Congestive heart failure is the most common cause of mortality in patients with end-stage renal disease (ESRD). Ultrasonic
tissue characterization with integrated backscatter offers a promising method for the noninvasive assessment of regional myocardial
contractile performance and fibrosis. The aim of this study was to investigate the effect of hemodialysis (HD) on myocardial
tissue characterization and left ventricular function in ESRD patients. We examined 26 patients with ESRD undergoing routine
HD (age 63 ± 12 years, duration of HD 9.2 ± 3.2 years) and 30 patients with essential hypertension (HT; 60 ± 10 years). Routine
echocardiographic parameters and the cyclic variation of ultrasonic integrated backscatter of the ventricular septum (CV-IBS)
were measured. Left ventricular mass index was significantly larger in patients with ESRD than in those with HT (217 ± 56
vs 146 ± 45 g/m2, P < 0.05). The indices for left ventricular diastolic function (E/A, the ratio of left ventricular peak early to late diastolic
filling velocity; DT, the deceleration time of the early diastolic filling) and CV-IBS had deteriorated significantly in patients
with ESRD before HD compared with those with HT (E/A, 0.6 ± 0.2 vs 0.9 ± 0.3, P < 0.05; DT, 228 ± 23 vs 184 ± 19 ms, P < 0.05; CV-IBS, 9.0 ± 1.3 vs 12.4 ± 0.9 dB, P < 0.05), possibly reflecting interstitial fibrosis. In patients with ESRD, HD reduced calculated left ventricular mass index
by 19% (before HD, 217 ± 56 vs immediately after HD, 176 ± 45 g/m2, P < 0.05) and CV-IBS by 19% (9.0 ± 1.3 vs 7.3 ± 1.1 dB, P < 0.05), that possibly reflected improvement of interstitial edema. HD also significantly improved indices for left ventricular
diastolic function (E/A, 0.6 ± 0.2 vs 0.9 ± 0.2, P < 0.05; DT, 228 ± 23 vs 188 ± 21 ms, P < 0.05). HD improves myocardial interstitial edema and left ventricular diastolic function in patients with ESRD. Noninvasive
assessment of ultrasonic tissue characterization is useful in defining the pathophysiological changes of ventricular myocardium
in patients with ESRD.
Received: December 17, 2001 / Accepted: April 19, 2002
Correspondence to O. Hirono 相似文献
We aimed to clarify the prognosis and pathophysiological parameters of low T3 syndrome in patients with heart failure (HF).
Methods and Results
Hospitalized patients with HF and euthyroidism (n?=?911) were divided into 2 groups on the basis of free triiodothyronine (FT3) serum levels: the normal FT3 group (FT3 ≥2.3 pg/mL; n?=?590; 64.8%) and the low FT3 group (FT3 <2.3 pg/mL; n?=?321; 35.2%). We compared post-discharge cardiac and all-cause mortality by means of Kaplan-Meier analysis and Cox proportional hazard analysis, and the parameters of echocardiography and cardiopulmonary exercise testing by means of Student t test. In the follow-up period of median 991 (interquartile range 534-1659) days, there were 193 all-cause deaths, including 88 cardiac deaths. Cardiac and all-cause mortality were higher in the low FT3 group (log-rank P < .01). Low FT3 was a predictor of cardiac death (hazard ratio 1.926, 95% confidence interval [CI] 1.268–2.927; P?=?.002) and all-cause death (hazard ratio 2.304, 95% CI 1.736–3.058; P < .001). Although left ventricular ejection fraction was similar between the groups, the low FT3 group showed lower peak VO2 (13.6 ± 4.6 vs 16.6 ± 4.4 mL·kg?1·min,?oneP < .001) and higher VE/VCO2 slope (36.5 ± 8.2 vs 33.0 ± 7.5; P?=?.001).
Conclusion
Low T3 syndrome in patients with HF is associated with higher cardiac and all cause-mortality. 相似文献
It is widely recognized that overt hyper- as well as hypothyroidism are potential causes of heart failure (HF). Additionally it has been recently reported that subclinical hypothyroidism (sub-hypo) is associated with atherosclerosis, development of HF, and cardiovascular death. We aimed to clarify the effect of sub-hypo on prognosis of HF, and underlying hemodynamics and exercise capacity.
Methods
We measured the serum levels of thyroid stimulating hormone (TSH) and free thyroxine (FT4) in 1100 consecutive HF patients. We divided these patients into 5 groups on the basis of plasma levels of TSH and FT4, and focused on euthyroidism (0.4 ≤ TSH ≤ 4 μIU/mL and 0.7 ≤ FT4 ≤ 1.9 ng/dL; n = 911; 82.8%) and sub-hypo groups (TSH > 4 μIU/mL and 0.7 ≤ FT4 ≤ 1.9 ng/dL; n = 132; 12.0%). We compared parameters of echocardiography, cardiopulmonary exercise testing, and cardiac catheterization, and followed up for cardiac event rate and all-cause mortality between the 2 groups.
Results
Although left ventricular ejection fraction did not differ between the 2 groups, the sub-hypo group had lower peak breath-by-breath oxygen consumption and higher mean pulmonary arterial pressure than the euthyroidism group (peak breath-by-breath oxygen consumption, 14.0 vs 15.9 mL/min/kg; P = 0.012; mean pulmonary arterial pressure, 26.8 vs 23.5 mm Hg, P = 0.020). In Kaplan-Meier analysis (mean 1098 days), the cardiac event rate and all-cause mortality were significantly higher in the sub-hypo group than those in the euthyroidism group (log rank, P < 0.01, respectively). In Cox proportional hazard analysis, sub-hypo was a predictor of cardiac event rate and all-cause mortality in HF patients (P < 0.05, respectively).
Conclusions
Sub-hypo might be associated with adverse prognosis, accompanied by impaired exercise capacity and higher pulmonary arterial pressure, in HF patients. 相似文献
BACKGROUND: A fulminant course can be difficult to predict at the onset of acute myocarditis, so the aim of the present study was to identify the predictive clinical symptoms/signs or laboratory findings. METHODS AND RESULTS: Thirty-nine patients with acute lymphocytic myocarditis, excluding 8 who manifested shock at admission, were studied. The fulminant group was defined as 12 patients who developed shock after admission, requiring intraaortic balloon pumping or percutaneous cardiopulmonary support, and the non-fulminant group comprised the 27 patients without shock. Various parameters at admission were compared between the 2 groups, together with multiple logistic regression analysis, excluding 6 patients with partially missing values. In the fulminant group, C-reactive protein (7.0 +/- 7.0 vs 2.3 +/- 2.2 mg/dl, p<0.01) and creatine kinase (1,147 +/- 876 vs 594 +/- 568 IU/L, p<0.05) concentrations were higher, intraventricular conduction disturbances were more frequent (9/12 vs 7/27 patients, p<0.01) and the left ventricular ejection fraction was lower (40.7 +/- 13.9 vs 50.1 +/- 10.6%, p<0.05) than in the non-fulminant group. In the multiple logistic regression analysis model with the presence/absence of a fulminant course considered as the independent variable, and C-reactive protein, creatine kinase, intraventricular conduction disturbances, and left ventricular ejection fraction as dependent variables, a high-risk group (expected proportion of fulminant course > or = 0.5) and a low-risk group (<0.5) could be differentiated. A fulminant course occurred in 9/13 (69%) patients in the high-risk group, but in only 2/20 (10%) patients in the low risk group (p<0.001). CONCLUSIONS: The risk of a fulminant course of acute myocarditis was high in patients with elevated C-reactive protein, and creatine kinase concentrations, decreased left ventricular ejection fraction, and intraventricular conduction disturbances at the time of admission. 相似文献
Background: The detailed mechanisms of knee osteoarthritis (OA) pain have not been clarified, but involvement of inflammatory cytokines such as tumor necrosis factor-alpha (TNF) has been suggested. The present study aimed to investigate the more detailed neurological involvement of TNF in joint pain using a TNF-knockout mouse OA model. Methods: The right knees of twelve-week-old C57BL/6J wild and TNF-deficient knockout (TNF-ko) mice (n=15, each group) were given a single intra-articular injection of 10 µg monoiodoacetate in 10 mL sterile saline. The left knees were only punctured as the control. Evaluations were performed immediately after the injection (baseline) and at 7, 14, and 28 days after the injection with a subsequent intra-articular injection of neurotracer into both knees. The animals were evaluated for immunofluorescence of the lumbar dorsal root ganglia (DRG) innervating the knee joints. The injected knees were observed macroscopically and mouse pain-related behaviors were scored. Results: Macroscopic observation showed similar knee OA development in both wild and TNF-ko mice. Calcitonin gene-related peptide (CGRP, a neuropeptide identified as a inflammatory pain-related biomarker) was significantly increased in DRG neurons innervating OA-induced knee joints with significantly less CGRP expression in TNF-ko animals. Pain-related behavior scoring showed a significant increase in pain in OA-induced joints, but there was no significant difference in pain observed between the wild and TNF-ko mice. Conclusions: The result of the present study indicates the possible association of TNF-alpha in OA pain but not OA development. 相似文献