Purpose: We investigated whether myocardial SPECT had additional usefulness to clinical, functional or surgical indices for the preoperative evaluation of cardiac risks in noncardiac surgery. Materials and Methods: 118 patients (M: F=66: 52, $62.7{\pm}10.5$ years) were studied retrospectively. Eighteen underwent vascular surgeries and 100 nonvascular surgeries. Rest T1-20l/ stress Tc-99m-MIBI SPECT was performed before operation and cardiac events (hard event: cardiac death and myocardial infarction; soft event: ischemic ECG change, congestive heart failure and unstable angina) were surveyed through perioperative periods ($14.6{\pm}5.6$ days). Clinical risk indices, functional capacity, surgery procedures and SPECT findings were tested for their predictive values of perioperative cardiac events. Results: Perioperative cardiac events occurred in 25 patients (3 hard events and 22 soft events). Clinical risk indices, surgical procedure risks and SPECT findings but functional capacity were predictive of cardiac events. Reversible perfusion decrease was a better predictor than persistent decrease, Multivariate analysis sorted out surgical procedure risk (p=0.0018) and SPECT findings (p=0.0001) as significant risk factors. SPECT could re-stratify perioperative cardiac risks in patients ranked with surgical procedures. Conclusion : We conclude that myocardial SPECT provides additional predictive value to surgical type risks as well as clinical indexes or functional capacity for the prediction of preoperative cardiac events in noncardiac surgery.
Introduction : Although myocardial ischemia tends to occur more frequently than can he documented in ventilated patients, it has not been well studied on the factors related to the occurrence of the ischemia. Methods : To investigate the related factors to ischemia development, a prospective study was done in 95 cases with consecutive 73 patients who had received mechanical ventilation(MV) in MICU. In addition to 24 h holter monitoring, echocardiogram, electrolytes, cardiac enzymes, hemodynamic, and gas exchange measurements were done within 24 h after initiation of MV in 69 cases. The measurements were repeated at weaning period in 26 cases. The ischemia was defined by the ST segment changes; up-sloping depression more than 1.5 mm or down-sloping or horizontal depression more than 1.0 mm from isoelectric baseline for 80 ms following J point. Results : Twelve patients(12.6% in 95 cases) developed ischemia in total. The incidence of ischemia development showed an increased tendency in the initial 24 hr after MV (15.9%) and in patients with left-sided heart failure found by echocardiogram (18.2%) compared with that of the weaning period (3.8%) and patients without heart failure (10.9%) (P=0.12, P=0.09, in each). There were no differences in APACHE III score, baseline ECG findings, electrolytes abnormalities, use of inotropics or bronchodilators, presence of sepsis or shock, mode of ventilation, and survival rate according to the development of ischemia. Maximal heart rates and mean arterial pressure also were not different between patients with ($137.2{\pm}30.9/min$, $82.5{\pm}15.9$ mm Hg) and without ischemia ($l29.5{\pm}29.7/min$, $83.8{\pm}17.6$ mm Hg). Conclusion : Although the incidence of myocardial ischemia was 12.6% in total, there were no clinically predictable factors to the development of ischemia during mechanical ventilation.
Chun, Sung Kook;Go, Kristina;Yang, Ming-Jim;Zendejas, Ivan;Behrns, Kevin E.;Kim, Jae-Sung
Toxicological Research
/
v.32
no.1
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pp.35-46
/
2016
No-flow ischemia occurs during cardiac arrest, hemorrhagic shock, liver resection and transplantation. Recovery of blood flow and normal physiological pH, however, irreversibly injures the liver and other tissues. Although the liver has the powerful machinery for mitochondrial quality control, a process called mitophagy, mitochondrial dysfunction and subsequent cell death occur after reperfusion. Growing evidence indicates that reperfusion impairs mitophagy, leading to mitochondrial dysfunction, defective oxidative phosphorylation, accumulation of toxic metabolites, energy loss and ultimately cell death. The importance of acetylation/deacetylation cycle in the mitochondria and mitophagy has recently gained attention. Emerging data suggest that sirtuins, enzymes deacetylating a variety of target proteins in cellular metabolism, survival and longevity, may also act as an autophagy modulator. This review highlights recent advances of our understanding of a mechanistic correlation between sirtuin 1, mitophagy and ischemic liver injury.
Cardiomyocyte apoptosis is initiated by various cellular insults and accumulated cardiomyocyte apoptosis leads to the pathogenesis of heart failure. Excessive reactive oxygen species (ROS) provoke apoptotic cascades. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme that converts cellular ROS into harmless products. In this study, we demonstrate that MnSOD is down-regulated upon hydrogen peroxide treatment or ischemia/reperfusion (I/R) injury. Enhanced expression of MnSOD attenuates cardiomyocyte apoptosis and myocardial infarction induced by I/R injury. Further, we show that miR-23a directly regulates the expression of MnSOD. miR-23a regulates cardiomyocyte apoptosis by suppressing the expression of MnSOD. Our study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. Our study provides a new method to tackling apoptosis related cardiac diseases.
Intramural hematoma of the aorta (IMH) is the precursor or a variant of a classic aortic dissection where hemorrhage occurs within the aorta wall in the absence of an initial intimal tear. IMH has a high rate of mortality and morbidity. The optimal therapy for IMH is uncertain, yet the involvement of the ascending aorta is usually considered as an indication for surgery due to the associated risk of rupture or cardiac tamponade. We report here on a case of a 71-year-old man who presented with syncope. Because of misdiagnosis, he underwent computed tomography (CT) after 5 hrs from arriving to the ER. Computed tomography of the aorta revealed intramural hematoma of the ascending aorta with cardiac tamponade. He also had vascular complications such as acute renal failure and visceral ischemia. We performed emergency graft replacement of the total arch and ascending aorta. He was discharged without complication on postoperative day 14.
Panax Ginseng C.A. Meyer has been known for hundreds of years as the most valuable drug having mysterious effects among all the herbal medicines and plants in Korea. Also, many experimental studies have been performed recently that the various effects were identified and applied clinically. So we attempted an experimental study on the effect of ginsenoside Rg1 mixtures in an isolated rat heart with the use of the Langendorff model. The objective of this study was to determine whether this ginsenoside Rg1 mixtures would protect the myocardial injury after ischemic arrest and reperfusion. Isolated rat hearts were allowed to equilibrate for 20 minutes and were then subjected to 15 minutes of normothermic ischemia. After this ischemic period, isolated rat hearts were allowed to reperfusion for 10 minutes(Ischemic Group). In other group , isolated rat hearts were perfused for 60 minutes continuously with normothermia( Normothermic Group). Hemodynamic and biochemical parameters such as heart rate, left ventricular pressure, +dp/dt max, coronary blood flow and cardiac enzymes were measured during initial perfusion, ischemia, reperfusion period (Ischemic group) and 20, 40 and 60 minutes after continuous perfusion(Normothermic group). After completion of the experiment, this data was evaluated and the following results were obtained. 1. Heart rates showed an increase in both ischemic and normothermic experimental groups, but statistically significant differences were not identified. 2. LVP(Left Ventricular Pressure) showed statistically significant differences in both ischemic and normothermic experimental groups(p<0.005, p<0.01). 3. +dp/dt max showed statistically significant differences in both ischemic and normothermic experimental groups(p<0.01, p<0.01). 4. There were no statistically significant differences in coronary blood flow and cardiac cenzymes in all groups, but experimental groups seemed to have better protection and recovery. These results suggest that ginsenoside Rg1 mixtures has a protective effect on the myocardial injury after ischemia and reperfusion.
Background: Effective strategies are dramatically needed to prevent and improve the recovery from myocardial ischemia and reperfusion (I/R) injury. Direct interactions between the mitochondria and endoplasmic reticulum (ER) during heart diseases have been recently investigated. This study was designed to explore the cardioprotective effects of gypenoside XVII (GP-17) against I/R injury. The roles of ER stress, mitochondrial injury, and their crosstalk within I/R injury and in GP-17einduced cardioprotection are also explored. Methods: Cardiac contractility function was recorded in Langendorff-perfused rat hearts. The effects of GP-17 on mitochondrial function including mitochondrial permeability transition pore opening, reactive oxygen species production, and respiratory function were determined using fluorescence detection kits on mitochondria isolated from the rat hearts. H9c2 cardiomyocytes were used to explore the effects of GP-17 on hypoxia/reoxygenation. Results: We found that GP-17 inhibits myocardial apoptosis, reduces cardiac dysfunction, and improves contractile recovery in rat hearts. Our results also demonstrate that apoptosis induced by I/R is predominantly mediated by ER stress and associated with mitochondrial injury. Moreover, the cardioprotective effects of GP-17 are controlled by the PI3K/AKT and P38 signaling pathways. Conclusion: GP-17 inhibits I/R-induced mitochondrial injury by delaying the onset of ER stress through the PI3K/AKT and P38 signaling pathways.
Decrease in cardiac function after open heart surgery is due to an ischemia induced myocardial damage during surgery, and ischemic preconditioning, a condition in which the myocardial damage does not accumulate after repeated episodes of ischemia but protects itself from damage after prolonged ischemia due to myocytes tolerating the ischemia, is known to diminish myocardial damage, which also helps the recovery of myocardium after reperfusion, and decreases incidences of arrythmia. Our study is performed to display the ischemic preconditioning and show the myocardial protective effect by applying cardioplegic solution to the heart removed from rat. Material and Method: Sprague-Dawley male rats were used, They were fixed on a modified isolated working heart model after cannulation. The reperfusion process was according to non-working and working heart methods and the working method was executed for 20 minutes in which the heart rate, aortic pressure, aortic flow and coronary flow were measured and recorded. The control group is the group which the extracted heart was fixed on the isolated working heart model, recovered by reperfusion 60 minutes after infusion and preserved in the cardioplegic solution 20 minutes after the working heart perfusion and aortic cross clamp, The thesis groups were divided into group I, which ischemic hearts that were hypoxia induced were perfused by cardioplegic solution and preserved for 60 minutes; group II, the cardioplegic solution was infused 45 seconds (II-1), 1 minutes (II-2), 3 minutes (II-3), after the ischemia induction, 20 minutes after working heart perfusion and aortic cross clamp; and group III, hearts were executed on working heart perfusion for 20 minutes and aortic cross clamp was performed for 45 seconds (III-1), 1minute (III-2), 3 minutes (III-3), reperfused for 2 minutes to recover the heart, and then aortic cross clamping was repeated for reperfusion, all the groups were compared based on hemodynamic performance after reperfusion of the heart after preservation for 60 minutes. Result: The recovery time until spontaneous heart beat was longer in groups I, II-3, III-2 and III-3 to control group (p<0.01). Group III-1 (p<0.05) had better results in terms of recovery in number of heart rates compared to control group, and recovered better compared to II-1 (p<0.05). The recovery of aortic blood pressure favored group III-1 (p<0.05) and had better outcomes compared with II-1 (p<0.01). Group III-1 also showed best results in terms of cardiac output (p<0.05) and group III-2 was better compared to II-2 (p<0.05). Group I (p<0.01) and II-3 (p<0.05) showed more cardiac edema than control group. Conclusion: When the effects of other organs are dismissed, protecting the heart by infusion of cardioplegic solution after enforcing ischemia for a short period of time before the onset of abnormal heart beats for preconditioning has a better recovery effect in the cardioplegic group with preconditioning compared to the cardioplegic solution itself. we believe that further study is needed to find a more effective method of preconditioning.
The purpose of the present study was to evaluate the expression of cardiac marker protein in rabbit cardiac tissue that was exposed to ischemic preconditioning (IPC), or ischemiareperfusion injury (IR) using two-dimensional gel electrophoresis (2DE) and matrix-assisted laser desorption ionization mass spectrometry (MALDI-MS). We compared 2DE gels of control (uninjured) cardiac tissue with those of IPC and IR cardiac tissue. Expression of one protein was detected in IR heart tissue, however the protein was not detected in the samples of control and IPC tissue. To further characterize the detected protein molecule, the protein in the 2D gel was isolated and subjected to trypsin digestion, followed by MALDI-MS. The protein was identified as myoglobin, which was confirmed also by Western blot analysis. These results are consistent with previous studies of cardiac markers in ischemic hearts, indicating myoglobin as a suitable marker of myocardial injury. In addition, the present use of multiple techniques indicates that proteomic analysis is an appropriate means to identify cardiac markers in studies of IPC and IR.
Journal of Institute of Control, Robotics and Systems
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v.8
no.8
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pp.691-697
/
2002
Myocardial ischemia is a disorder of cardiac function caused by insuficient blood flow to the muscle tissue of the heart. We can diagnose myocardial ischemia by observing the change of ST-segment, but this change is temporary. Our primary purpose is to detect the temporary change of the 57-segment automatically In the signal processing, the wavelet transform decomposes the ECG(electrocardiogram) signal into high and low frequency components using wavelet function. Recomposing the high frequency bands including QRS complex, we can detect QRS complex more easily. Amplitude comparison method is adopted to detect QRS complex. Reducing the effect of noise to the minimum, we grouped ECG by 5 data and compared the amplitude of maximum value. To recognize the ECG .signal pattern, we adopted the polynomial approximation partially and statistical method. The polynomial approximation makes possible to compare some ECG signal with different frequency and sampling period. The ECG signal is divided into small parts based on QRS complex, and then, each part is approximated to the polynomials. After removing the distorted ECG by calculating the difference between the orignal ECG and the approximated ECG for polynomial, we compared the approximated ECG pattern with the database, and we detected and classified abnormality of ECG.
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