Introduction: Central aortic pressure waveform analyses can provide clinically relevant information beyond conventional brachial blood pressure (BP) assessment. This waveform can be reproduced non-invasively through application of a general transfer function (GTF) on a peripheral waveform, as conventionally performed by applanation tonometry. Photoplethysmography (PPG) is an alternate approach, however, differences in measurement site and modality demand the use of a transfer function (TF) specific for those differences. This study aims to compare central aortic waveform features generated from radial tonometry (reference) using a proprietary GTF with a central aortic waveform and its features generated from a simultaneous fingertip PPG measurement using a selective method where one of three different TFs is chosen based on the input signal harmonic profile. Methods: Brachial BP was measured in triplicate under resting conditions and was used for subsequent calibration. Multiple simultaneous radial tonometry (SphygmoCor CvMS) and fingertip PPG measurements were then performed in individual participants (n=21, 10 females, age: 39±16 years). Measurements were converted into central aortic waveforms with their respective TFs. Twenty central aortic pressure waveform parameters were compared through correlation analysis, Bland-Altman plots, and a repeated measure mixed-effects ANOVA model. Central aortic waveform shape was compared using the root-mean-squared error (RMSE). Results: Correlation (r) of PPG-derived parameters with radially tonometry derived central aortic parameters were high ranging from 0.79 to 0.99. Mean differences of pressure-related parameters were within 1.3 mmHg and differences of time-related parameters ranged from –2.2 to 3.4%. Whilst some parameters were statistically different these differences are not physiologically meaningful. Central aortic waveform shape had an average RMSE of 1.8±0.9%. Conclusion: Fingertip PPG derived central aortic waveform parameters using a novel selective TF were comparable to central aortic waveform features derived from radial tonometry using a previously validated GTF.

Introduction: Transcatheter Aortic Valve Implantation (TAVI) has emerged as a common and effective treatment for patients with severe aortic stenosis. Changes in systemic blood pressure after TAVI have been described, yet their prognostic value are not established. Thus, we aimed to examine the association of the peri-procedural changes in systolic blood pressure and in pulse pressure on clinical outcomes after the procedure. Methods: A retrospective study of consecutive patients who underwent TAVI procedure in our medical center. We assessed the effect of the periprocedural changes in blood pressure measurements on mortality, acute myocardial infarction, stroke and hospitalizations at 1-year and on the combined outcome of death, myocardial infarction and stroke at one year following the procedure. Results: Our cohort included 455 patients (44% males). Of them, 343 patients (75.4%) have raised the systolic blood pressure (SBP) immediately after the procedure. Patients who raised SBP had a significantly higher rate of the 1-year composite outcome, compared to patients who did not raise SBP following the procedure (43 [13%] vs 6 [5.4%], respectively, p=0.033). After adjustment for age and sex, the postprocedural increase in SBP was significantly associated with the composite outcome, with a hazard ratio of 2.42, 95% CI 1.03-5.7. Conclusion: An immediate increase in SBP after TAVI is associated with worse 1-year clinical cardiovascular outcomes.

Introduction: Acute hemorrhage decreases blood pressure (BP) and sometimes causes hypovolemic shock. At this time, peripheral arteries are supposed to contract and increase peripheral vascular resistance to raise BP. However, there has not been an adequate index of a degree of arterial stiffness. We assessed changes in arterial stiffness during rapid bleeding using new BP-independent vascular indices, aBeta and ifBeta, determined by applying the cardio-ankle vascular index theory to the elastic (aorta) and muscular (common iliac-femoral) arteries, respectively, in rabbits. Methods: Eleven Japanese white male rabbits were fixed at the supine position under pentobarbital anesthesia. Fifteen percent of the total blood volume was depleted at a rate of 2 mL/kg/min for 6 min; 15 min later, the withdrawn blood was re-transfused at the same rate. Pressure waves at the origin of the aorta (oA), distal end of the abdominal aorta (dA), distal end of the left common iliac artery (fA), and flow waves at oA were measured simultaneously. Beta was calculated using the following formula: beta = 2ρ/PP × ln(SBP/DBP) × PWV2, where ρ, SBP, DBP, and PP are blood density, systolic, diastolic, and pulse pressures, respectively. aBeta, ifBeta, and aortic-iliac-femoral beta (aifBeta) were calculated using aPWV, ifPWV, and aifPWV, respectively. Results: BP declined significantly at oA, dA, and fA during the acute bleeding. aBeta and aifBeta increased significantly from 3.7 and 5.0 before the bleeding (control) to 5.0 (about 34%) and 6.3 (about 26%) on average, while ifBeta decreased significantly from 20.5 before the bleeding to 17.1 (about 17%) after the completion of the bleeding. Reverse reactions of those indices were observed by transfusing the removed blood. Conclusion: Total arterial stiffness (aifBeta) increased; however, the elastic and muscular arteries stiffened and softened during the bleeding, respectively. These results would give useful diagnostic information during fall in BP.

Background: Pulmonary hypertension (PH) is a debilitating condition characterized by elevated pulmonary arterial pressure and progressive vascular remodeling, leading to exercise intolerance. The progression of PAH is regulated at a cellular and molecular level which influences various physiological processes. Exercise plays an important role in improving function in PH. Although the signalling pathways that regulate cardio-protection through exercise have not been fully understood, the positive impact of exercise on the various physiological systems are well established. Summary: Exercise has emerged as a potential adjunctive therapy for PH, with growing evidence supporting its beneficial effects on various aspects of the disease pathophysiology. This review highlights the contributions of cellular and molecular pathways and physiological processes to exercise intolerance. Preclinical studies have provided insight into the mechanisms underlying exercise-induced improvements in PH which are modulated through improvements in endothelial function, inflammation, oxidative stress, and mitochondrial function. Along with preclinical studies, various clinical studies have demonstrated that exercise training can lead to significant improvements in exercise capacity, hemodynamics, quality of life, and functional status. Moreover, exercise interventions have been shown to improve skeletal muscle function, and enhance pulmonary vascular remodeling, contributing to overall disease management. Further research efforts aimed at better understanding the role of exercise in PH pathophysiology and refining exercise interventions are warranted to realize its full potential in the management of this complex disease. Key messages: Despite the promising benefits of exercise in PH, several challenges remain, including the optimal intensity, duration, and type of exercise training, as well as patient selection criteria and long-term adherence. Additionally, the mechanisms underlying the observed improvements require further elucidation to optimize exercise protocols and personalize treatment strategies. Nonetheless, exercise represents a promising therapeutic approach that can complement existing pharmacological therapies and improve outcomes in PH patients.

Background: Enhanced regenerative therapeutic strategies are required to treat intractable ischemic heart disease. Summary: Since the discovery of putative endothelial progenitor cells (EPCs) in 1997, many studies have focused on their extraction, ex vivo processing, and autotransplantation under ischemic conditions. Nonetheless, numerous randomized clinical trials involving thousands of patients have yielded only marginal treatment effects, highlighting the need for advances regarding insufficient dosage and complex ex vivo processing. The prevailing paradigm of cellular differentiation highlights the potential of direct cellular reprogramming, which paves the way for in situ reprogramming. In situ reprogramming holds the promise of significantly enhancing current therapeutic strategies, yet its success hinges on the precise targeting of candidate cells for reprogramming. In this context, the spleen emerges as a pivotal “in situ reprogramming hub,” owing to its dual function as both a principal site for nanoparticle distribution and a significant reservoir of putative EPCs. The in situ reprogramming of splenic EPCs offers a potential solution to overcome critical challenges, including the aforementioned insufficient dosage and complex ex vivo processing. Key Messages: This review explores the latest advancements in EPC therapy and in situ reprogramming, spotlighting a pioneering study that integrates those two strategies with a specific focus on the spleen. Such an innovative approach will potentially herald a new era of regenerative therapy for ischemic heart disease.

Background: Patients with spinal cord injuries (SCIs) are at a greater risk for the development of cardiovascular diseases (CVDs) than able-bodied individuals due to the high risk of endothelial dysfunction. Summary: For instance, patients with SCIs lose autonomic control of the heart and vasculature, which results in severe fluctuations in blood pressure. These oscillations between hypotension and hypertension have been shown to damage blood vessel endothelial cells and may contribute to the development of atherosclerosis. Furthermore, the loss of skeletal muscle control results in skeletal muscle atrophy and inward remodeling of the conduit arteries. It has been shown that blood vessels in the legs are chronically exposed to high shear, while the aorta experiences chronically low shear. These alterations to shear forces may adversely impact endothelial vasodilatory capacity and promote inflammatory signaling and leukocyte adherence. Additionally, microvascular endothelial vasodilatory capacity is impaired in patients with an SCI, and this may precede changes in conduit artery endothelial function. Finally, due to immobility and a loss of skeletal muscle mass, patients with SCIs have a higher risk of metabolic disorders, inflammation, and oxidative stress. Key Messages: Collectively, these factors may impair endothelium-dependent vasodilatory capacity, promote leukocyte adhesion and infiltration, promote the peroxidation of lipids, and ultimately support the development of atherosclerosis. Therefore, future interventions to prevent CVDs in patients with SCIs should focus on the management of endothelial health to prevent endothelial dysfunction and atherosclerosis.

Introduction: Despite its efficacy, conventional center-based cardiac rehabilitation has several limitations which have led to the emergence of home-based programs and intensive cardiac rehabilitation as alternative methods for overcoming these limitations. Alternative methods for primary prevention have been recommended for similar reasons. Lifestyle modification is considered key to success in both primary and secondary prevention. Therefore, this primary prevention study aimed to investigate the efficiency of intensive lifestyle education and home-based programs involving unstructured exercise in urban forests to prevent coronary artery disease (CAD). The availability of urban forests as preventive exercise environments was also examined. Methods: Patients with risk factors for CAD participated in primary prevention using either FBEG (forest-based exercise group (FBEG, n = 11) or CBEG (center-based exercise group (CBEG, n = 17) for 12 weeks. The FBEG was provided with intensive residential lifestyle education and followed a home program that included performing exercise in an urban forest. The CBEG followed a conventional supervised exercise program at a fitness facility. Changes in body composition, cardiometabolic variables, and functional capacity were tested using a 2-way repeated ANOVA measurement. An independent t-test was used to examine the differences in weekly energy expenditure between the two groups. Results: Significant within-group differences were identified in body composition, cardiometabolic variables, and the 10-yr probability of CAD in both groups. However, the functional capacity, weekly energy expenditure, and attendance rate showed between-group differences, with superiority in the FBEG. Conclusion: Intensive lifestyle education and subsequent home-based programs with unstructured exercise in the forest were as effective as a conventional center-based program, with superiority in terms of the change of some variables. Intensive education on experiencing and habituating a healthy lifestyle seemed to play an important role in improving motivation.

Background: Exercise training elicits indubitable positive adaptation in microcirculation in health and disease populations. An inclusive overview of the current knowledge regarding the effects of exercise on microvascular function consolidates an in-depth understanding of microvasculature. Summary: The main physiological function of microvasculature is to maintain optimal blood flow regulation to supply oxygen and nutrition during elevated physical demands in the cardiovascular system. There are several cellular and molecular alterations in resistance vessels in response to exercise intervention, an increase in nitric oxide-mediated vasodilation through the regulation of oxidative stress, inflammatory response, and ion channels in endothelial cells, thus increasing myogenic tone via voltage-gated Ca2+ channels in smooth muscle cells. Key Messages: In the review, we postulate that exercise should be considered a medicine for people with diverse diseases through a comprehensive understanding of the cellular and molecular underlying mechanisms in microcirculation through exercise training.

Background: Despite advancements in coronary artery disease (CAD) treatment with drug-eluting stent, its morbidity and mortality remain high. In context, intravascular imaging-guided percutaneous coronary intervention (PCI) is increasingly recommended for better clinical outcomes in patient with CAD. Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS), as one of the intravascular imaging methods, is effective in detecting lipid-rich plaques, which is crucial for identifying high-risk or vulnerable plaques employing near-infrared light. High lipid core burden, as identified by NIRS-IVUS, correlates with an increased risk of adverse cardiac events and shows varying degrees of efficacy in plaque management and event prevention. Summary: This article addresses about how NIRS-IVUS can be used to predict event of CAD. The study highlights the crucial role of NIRS-IVUS in predicting future cardiovascular events. Findings indicate that the presence of high lipid core burden is related to increased risks of periprocedural myocardial infarction and reduced coronary flow during PCI. The study also outlines the predictive value of NIRS-IVUS in non-culprit lesions, where plaques with high lipid core burden significantly increase the occurrence of major adverse cardiac events as demonstrated in the PROSPECT II trial. In terms of therapeutic strategies, the study reviews the effectiveness of high-intensity lipid-lowering strategies in stabilizing vulnerable plaques, as evidenced in trials such as the YELLOW and PACMAN AMI trials. Key Messages: NIRS-IVUS emerges as a valuable diagnostic tool in treating CAD. It effectively identifies vulnerable plaques and aids in predicting and preventing future adverse cardiac events. However, to enhance its practicality and promote widespread adoption in clinical settings, further long-term outcome research of NIRS-IVUS-guided PCI is necessary. These efforts can potentially make NIRS-IVUS a more accessible and indispensable tool in cardiovascular disease management.

Proactive risk management program is essential to maintain the quality and safety of patient care, treatment, and services within a healthcare system. According to the Joint Commission, hospitals need to adopt a proactive approach for risk management and develop risk mitigation strategies to reduce or eliminate the potentially harmful impact of possible risk. There are multiple tools that can be used for proactive analysis. Leaders of Evercare hospital Dhaka selected Healthcare FMEA tool to identify the potential failure modes in the current medication management process as it is one of the complex and high processes in healthcare settings. A multidisciplinary Healthcare FMEA team was formed comprising physician, nurse, pharmacist, quality, IT personnel and senior managements of EHD to conduct Healthcare FMEA. After completing Healthcare FMEA, twenty failure modes(n-20) and fifty-nine potential causes(n-59) of failure modes were detected in existing medication management process of EHD. The hazardous score was Two hundred & seventeen (n-217). There were Twelve major failures modes with higher hazardous score. Healthcare FMEA team members decided to eliminate major failures and actions were taken to control these failures. The main objective of this study is to maintain the medication error of EHD within the target (2/1000 patient days) by implementing required strategies and redesigning existing medication management process. The limitation of this study was it is a time-consuming process, it only helps to identify the possibilities of fail; it does not eliminate them, additional efforts are required to develop corrective action. Pulse Vol.15, 2023 P: 28-33