Analysis of Cardiac Events and the Subsequent Impact for Geriatric Patients Undergoing Hip Fracture Surgeries.

Perioperative complications, particularly cardiac events, compromised surgical outcomes for geriatric patients. This retrospective study intended to investigate the occurrence and subsequent impact of cardiac events for geriatric patients undergoing hip fracture surgeries. We collected 607 patients undergoing hip fracture surgeries from January 2017 to December 2022 that received transthoracic echocardiography (TTE) pre-operatively to screen for cardiac abnormalities. Except for demographic characteristics, the researchers recorded fracture type, surgical method, American Society of Anesthesiologists (ASA) class, anesthesia type, perioperative cardiac events, and in-hospital mortality. Statistical analysis was performed using SPSS 22.0 statistics software. Throughout the whole course of the study, 16 postoperative cardiac events occurred. The cardiac events included ten arrhythmias, three acute myocardial infarctions, two heart failures, and one sudden death. Notably, 12 of 16 patients with cardiac events presented with abnormal findings on TTE, except 15 of them had a history of cardiac disease. This study disclosed 93.7% of cardiac events developed in patients with a history of cardiovascular disease. Among patients that experienced cardiac events, 75% of patients had abnormal echocardiographic findings. Pre-operative transthoracic echocardiography deserves a recommendation for geriatric patients with histories of cardiac diseases undergoing hip fracture surgeries to detect the risk of developing cardiac events earlier.

Clinical Significance of Electronegative Low-Density Lipoprotein Cholesterol in Atherothrombosis.

Despite the numerous risk factors for atherosclerotic cardiovascular diseases (ASCVD), cumulative evidence shows that electronegative low-density lipoprotein (L5 LDL) cholesterol is a promising biomarker. Its toxicity may contribute to atherothrombotic events. Notably, plasma L5 LDL levels positively correlate with the increasing severity of cardiovascular diseases. In contrast, traditional markers such as LDL-cholesterol and triglyceride are the therapeutic goals in secondary prevention for ASCVD, but that is controversial in primary prevention for patients with low risk. In this review, we point out the clinical significance and pathophysiological mechanisms of L5 LDL, and the clinical applications of L5 LDL levels in ASCVD can be confidently addressed. Based on the previously defined cut-off value by receiver operating characteristic curve, the acceptable physiological range of L5 concentration is proposed to be below 1.7 mg/dL. When L5 LDL level surpass this threshold, clinically relevant ASCVD might be present, and further exams such as carotid intima-media thickness, pulse wave velocity, exercise stress test, or multidetector computed tomography are required. Notably, the ultimate goal of L5 LDL concentration is lower than 1.7 mg/dL. Instead, with L5 LDL greater than 1.7 mg/dL, lipid-lowering treatment may be required, including statin, ezetimibe or PCSK9 inhibitor, regardless of the low-density lipoprotein cholesterol (LDL-C) level. Since L5 LDL could be a promising biomarker, we propose that a high throughput, clinically feasible methodology is urgently required not only for conducting a prospective, large population study but for developing therapeutics strategies to decrease L5 LDL in the blood.

Pulmonary hypertension in patients on chronic hemodialysis and with heart failure.

Pulmonary hypertension (PH) is linked to chronic kidney disease. However, few studies have examined the prevalence, risk factors, or outcomes of PH in patients with chronic hemodialysis and concomitant heart failure. This retrospective cohort study enrolled 160 patients with a history of acute decompensated heart failure after maintenance hemodialysis therapy. All patients were prospectively observed until December 2013 or death. PH was defined as pulmonary artery systolic pressure >35 mmHg, as determined through echocardiography. Fifty-one (32%) patients had PH, more of whom were female (70% vs. 52%, P = 0.04). The patients with PH had a lower body mass index (21.8 vs. 23.0, P = 0.03), higher cardiothoracic ratio (55% vs. 52%, P = 0.006), larger left atrium (38.5 vs. 35.7 mm, P = 0.01), and an increased proportion of mitral regurgitation (MR) (73% vs. 38%, P < 0.001) compared with the patients who did not have PH. In the multivariate regression analysis, MR was associated most strongly with PH (odds ratio 3.75, 95% confidence interval [CI]: 1.67-8.43, P = 0.001). In the multivariate Cox proportional hazard models, PH was related independently to all-cause mortality (hazard ratio [HR], 3.11; 95% CI, 1.53-6.31; P = 0.002) and combined cardiovascular events (HR, 2.71; 95% CI, 1.66-4.44; P < 0.001) after the model was adjusted for conventional cardiovascular risk factors. PH is related to MR and independently associated with increased all-cause mortality and cardiovascular events in patients with chronic hemodialysis and heart failure.

A xanthine-derivative K(+)-channel opener protects against serotonin-induced cardiomyocyte hypertrophy via the modulation of protein kinases.

This study investigated whether KMUP-1, a xanthine-derivative K(+) channel opener, could prevent serotonin-induced hypertrophy in H9c2 cardiomyocytes via L-type Ca(2+) channels (LTCCs). Rat heart-derived H9c2 cells were incubated with serotonin (10 µM) for 4 days. The cell size increased by 155.5%, and this was reversed by KMUP-1 (≥1 µM), and attenuated by the LTCC blocker verapamil (1 µM) and the 5-HT2A antagonist ketanserin (0.1 µM), but unaffected by the 5-HT2B antagonist SB206553. A perforated whole-cell patch-clamp technique was used to investigate Ca(2+) currents through LTCCs in serotonin-induced H9c2 hypertrophy, in which cell capacitance and current density were increased. The LTCC current (ICa,L) increased ~2.9-fold in serotonin-elicited H9c2 hypertrophy, which was attenuated by verapamil and ketanserin, but not affected by SB206553 (0.1 µM). Serotonin-increased ICa,L was reduced by KMUP-1, PKA and PKC inhibitors (H-89, 1 µM and chelerythrine, 1 µM) while the current was enhanced by the PKC activator PMA, (1 µM) but not the PKA activator 8-Br-cAMP (100 µM), and was abolished by KMUP-1. In contrast, serotonin-increased ICa,L was blunted by the PKG activator 8-Br-cGMP (100 µM), but unaffected by the PKG inhibitor KT5823 (1 µM). Notably, KMUP-1 blocked serotonin-increased ICa,L but this was partially reversed by KT5823. In conclusion, serotonin-increased ICa,L could be due to activated 5-HT2A receptor-mediated PKA and PKC cascades, and/or indirect interaction with PKG. KMUP-1 prevents serotonin-induced H9c2 cardiomyocyte hypertrophy, which can be attributed to its PKA and PKC inhibition, and/or PKG stimulation.

Comparison of automated 4D-MSPECT and visual analysis for evaluating myocardial perfusion in coronary artery disease.

The aim of this study was to assess the reproducibility and diagnostic performance for coronary artery disease (CAD) of an automated software package, 4D-MSPECT, and compare the results with a visual approach. We enrolled 60 patients without previously known CAD, who underwent dual-isotope rest Tl-201/stress Tc-99m sestamibi myocardial perfusion imaging and subsequent coronary angiography within 3 months. The automated summed stress score (A-SSS), summed rest score (A-SRS) and summed difference score (A-SDS) were obtained using a 17-segment five-point scale model with 4D-MSPECT. For intraobserver and interobserver variability assessment, automated scoring was done by a nuclear medicine physician twice and by a nuclear medicine technologist. The visual summed stress score (V-SSS), summed rest score (V-SRS), and summed difference score (V-SDS) were obtained by consensus of two nuclear medicine physicians. The intraobserver and interobserver agreements of automated segmental scores were excellent. The intraobserver and interobserver summed scores also correlated well. Agreements between visual and automated segmental scores were moderate (weighted kappa of 0.55 and 0.50 for stress and rest images, respectively). Correlations between automated and visual summed scores were high, with correlation coefficients of 0.89, 0.85 and 0.82 for SSS, SRS and SDS, respectively (all p < 0.001). The receiver operating characteristic area under the curve for diagnosis of CAD by V-SSS, V-SDS, A-SSS and A-SDS were 0.78 +/- 0.06, 0.87 +/- 0.05, 0.84 +/- 0.05 and 0.90 +/- 0.04, respectively. A-SDS had better diagnostic performance than A-SSS and V-SSS (p = 0.043 and p = 0.032, respectively), whereas there was no statistically significant difference between A-SDS and V-SDS (p = 0.56). Using V-SDS > or = 2 as a diagnostic threshold, the sensitivity, specificity, and accuracy for CAD were 83.7%, 76.5% and 81.7%, respectively. Using A-SDS > or = 3 as a diagnostic threshold, the sensitivity, specificity, and accuracy for CAD were 79.1%, 82.4% and 80.0%, respectively. In conclusion, the reproducibility of automated semiquantitative analysis with 4D-MSPECT was excellent. The diagnostic performance of automated semiquantitative analysis with 4D-MSPECT was comparable with the visual approach.

The association of silent coronary artery disease and metabolic syndrome in Chinese with type 2 diabetes mellitus.

OBJECTIVES: Cardiovascular diseases account for approximately 75% of the deaths that occur in patients with diabetes. Because the clinical signs of coronary artery disease (CAD) in diabetic patients are hard to detect and routine screening is costly, it would be of great benefit to try to either prevent CAD from occurring or to detect it early and provide optimal care. Therefore, we analyzed the risk factors that might predict CAD in type 2 diabetes mellitus (T2DM) patients with no classical cardiac ischemic symptoms. METHODS: Using a resting 12-lead ECG, exercise treadmill test, or thallium myocardial scintigraphy with exercise testing and dipyridamole injection, we screened diabetic patients already enrolled in a disease management program for possible CAD. We used diagnostic coronary angiography to confirm its presence. The definition and criteria of metabolic syndrome we used were modified from those outlined by the WHO classification and criteria of NCEP-ATP III. RESULTS: A total of 850 T2DM patients without clinical and electrocardiographic evidence of CAD were studied. Three hundred and sixty-eight asymptomatic patients with normal resting ECG were examined by exercise ECG test or thallium scintigraphy examination. Sixty patients considered to have a strong positive test or significant thallium myocardial ischemia received a diagnostic coronary angiography. Fifty-one were found to have significant coronary artery stenosis; 9 showed no significant ischemic lesion. While gender, patients' age, known diabetes duration, serum uric acid level, smoking status, and the presence of WHO-metabolic syndrome defined hypertension and nephropathy were associated with silent CAD, logistic regression analysis found that the only predictor of silent CAD was the presence of nephropathy. The components of NCEP-ATP III-metabolic syndrome were not found to be associated with silent CAD. CONCLUSIONS: A considerable proportion of T2DM patients have silent CAD. A diabetic patient with incipient or overt nephropathy should be examined for the presence of CAD. The definition of metabolic syndrome may be modified for early detection of CAD in patients with T2DM.

Differential effects of adenosine on antegrade fast pathway, antegrade slow pathway, and retrograde fast pathway in atrioventricular nodal reentry.

Adenosine has a potent negative dromotropic effect. However, comparative effects of adenosine on the three pathways of atrioventricular (AV) nodal reentry remain unclear. In this study, we sought to determine the effects of adenosine on the antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT). Twenty patients with common slow-fast AVNRT (mean cycle length 360 +/- 49 ms) were studied. The effects of adenosine on the antegrade slow pathway and on the retrograde fast pathway conduction were determined during sustained AVNRT and constant right ventricular pacing at identical cycle lengths (mean 360 +/- 49 ms), respectively. Incremental doses of adenosine were rapidly administered: initial dose of 0.5 mg, followed by stepwise increases of 0.5 or 1.0 mg given at 5-min intervals until termination of AVNRT or second-degree ventriculoatrial block occurred. After the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation, the effect of adenosine on the antegrade fast pathway conduction was evaluated. The dose-response curve of adenosine and the dose of adenosine required to produce AV or ventriculoatrial block among the representative three conduction pathways were compared. The dose-response curve for the effect of adenosine on the antegrade fast pathway lies to the left and upward to that of the effect of adenosine on the antegrade slow pathway which in turn lies to the left and upward to that of the retrograde fast pathway. The mean dose of adenosine required to produce conduction block at antegrade fast, antegrade slow, and retrograde fast pathways were 1.4 +/- 0.5, 4.2 +/- 1.6, and 8.5 +/- 2.6 mg, respectively (p < 0.01). Adenosine has a differential potency to depress antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AVNRT. The depressant effect of adenosine on the antegrade fast pathway is more potent than that on the antegrade slow pathway which in turn is more potent than that on the retrograde fast pathway conduction.

Simple Way to Resolve the Range Ambiguity.

PURPOSE: The purpose of this study was to test the hypothesis that with the range gate fixed, random adjustment of the pulse repetition frequency will offer a rapid and accurate way to avoid misinterpretation of range ambiguity. BACKGROUND: Traditionally, to avoid the misdiagnosis of Doppler artifacts caused by range ambiguity, time must be spent on checking the flow patterns in the calculated phantom range gates. METHODS: Twenty-four patients (mean age 64 +/- 15 years, 15 men and nine women) with mitral regurgitation were included in the study. Pulsed Doppler evaluation was performed with sample volume initially at the shallow left ventricle and then, along the direction of ultrasonic beam, at the calculated range gate distal to the mitral valve to search for the high velocity Doppler signal. The highest velocity scale was initially selected. After detection of high velocity signal, the velocity scale was lowered to achieve the lower pulse repetition frequency. RESULTS: For all patients, a high velocity regurgitant Doppler signal could be recorded both distal to the mitral valve and at the shallow left ventricle. Such signal persisted at the range gate distal to the mitral valve but disappeared at the range gate at the shallow left ventricle after manual adjustment of the velocity scale. The sensitivity, specificity, and accuracy of disappearance of the high velocity Doppler signal after adjustment of the pulse repetition frequency for confirmation of a phantom phenomenon are 100%, 100%, and 100%, respectively. CONCLUSIONS: Without the necessity of exact information about the pulse repetition frequency used, random adjustment of the pulse repetition frequency for the selected gate range is a rapid and exact method for initial differentiation of in situ from phantom signal in pulsed Doppler echocardiography.