Clinical Data Analysis for Prediction of Cardiovascular Disease Using Machine Learning Techniques

Cardiovascular disease is difficult to detect due to several risk factors, including high blood pressure, cholesterol, and an abnormal pulse rate. Accurate decision-making and optimal treatment are required to address cardiac risk. As machine learning technology advances, the healthcare industry’s clinical practice is likely to change. As a result, researchers and clinicians must recognize the importance of machine learning techniques. The main objective of this research is to recommend a machine learning-based cardiovascular disease prediction system that is highly accurate. In contrast, modern machine learning algorithms such as REP Tree, M5P Tree, Random Tree, Linear Regression, Naive Bayes, J48, and JRIP are used to classify popular cardiovascular datasets. The proposed CDPS’s performance was evaluated using a variety of metrics to identify the best suitable machine learning model. When it came to predicting cardiovascular disease patients, the Random Tree model performed admirably, with the highest accuracy of 100%, the lowest MAE of 0.0011, the lowest RMSE of 0.0231, and the fastest prediction time of 0.01 seconds.

Statistical Validation of Cardiovascular Digital Biomarkers Towards Monitoring the Cardiac Risk in COPD: A Lyfas Case Study

Background: Mobile health (mHealth) is gaining popularity due to its pervasiveness. Lyfas is a smartphone-based optical biomarker instrument catering to mHealth. It captures the Pulse Rate Variability (PRV) and its associated digital biomarkers from the index finger capillary circulation using the principle of arterial photoplethysmography. PRV surrogates for the Cardiovascular Autonomic Modulation (CvAM) and provides a snapshot of psychophysiological homeostasis of the body. Objective: The paper investigates the roles of (a) physiological factors, e.g., Age, Duration of illness, Heart Rate (HR), Respiration Rate (RR), SpO2 level, and (b) popular digital biomarkers, such as SDNN, LF/HF, RMSSD, pNN50, SD1/SD2 to evaluate the cardiac risk. The paper hypothesizes that low FEV1, which is another physiological factor, plays a critical role in defining such risk. Method: A total of 50 males and females each, suffering from Chronic Obstructive Pulmonary Disease (COPD) took the Lyfas test after appropriate ethical measures. Data, thus collected by Lyfas had been statistically analyzed using histogram plots and Kolmogorov-Smirnov test for normality check, Pearson's Correlations (PC) to measure the strength of associations, and linear regressions to test the goodness of fit of the model. Results: Positive PCs are noted between (a) RMSSD and SDNN ('very high'-females: 0.86 and males: 0.91), (b) pNN50 and RMSSD (PC: moderate 0.46), (c) pNN50 and SDNN (PC: moderate 0.44), (d) Duration of illness and Age ('high'-females: 0.71 and males: 0.77), and (e) Age and RR ('high'-females: 0.67, males: 0.53). Negative PC is noted between (a) LF/HF and FEV1 ('moderately high'-males 0.42) and (b) LF/HF and SpO2 ('moderately high'-males 0.30). Although the R2 values are not so encouraging (most are < 0.5), yet, the models are statistically significant (p-values 0.0336; CI 95%). Conclusion: The paper concludes that Lyfas may be used to predict the cardiac risk in COPD patients based on the LF/HF values correlated to SpO2 and FEV1 levels.

Acute Nonatherosclerotic Coronary Thromboembolism Presenting with an Inferior STEMI in a Patient on Oral Contraception

Background. Direct coronary embolism in the setting of oral contraceptive pill (OCP) use is a rare adverse effect. It is known for OCP to increase the risk of thrombosis; however, leading to an inferior ST elevated myocardial infarction (STEMI) due to an acute occlusive embolism is a rare entity. Coronary embolism occurs in about 3% of patients with acute coronary syndrome. Case Report. We present a case of a young 41-year-old female with a past medical history significant for dysfunctional uterine bleeding on oral contraceptive pills, who presented to the hospital with chest pain. Her workup was significant for troponin elevation and an electrocardiogram showing inferior ST elevations. The patient was taken emergently to the cardiac catheterization lab. A coronary angiogram revealed a coronary thrombus involving the distal left main and proximal left anterior descending (LAD) with no evidence of atherosclerotic disease. The patient subsequently received anticoagulation therapy leading to complete resolution of symptoms and ST elevations. Conclusion. Coronary embolism is rare and often not considered in the differential of acute coronary syndrome. It is of utmost importance for clinicians to keep a wide differential of nonatherosclerotic causes of STEMI especially when the patient is young, without significant cardiac risk factors.

Cardiac Risk Factors for Stroke: A Comprehensive Mendelian Randomization Study

Background and Purpose: Observational studies suggest an association of stroke with cardiac traits beyond atrial fibrillation, the leading source of cardioembolism. However, controversy remains regarding a causal role of these traits in stroke pathogenesis. Here, we leveraged genetic data to systematically assess associations between cardiac traits and stroke risk using a Mendelian Randomization framework. Methods: We studied 66 cardiac traits including cardiovascular diseases, magnetic resonance imaging–derived cardiac imaging, echocardiographic imaging, and electrocardiographic measures, as well as blood biomarkers in a 2-sample Mendelian Randomization approach. Genetic predisposition to each trait was explored for associations with risk of stroke and stroke subtypes in data from the MEGASTROKE consortium (40 585 cases/406 111 controls). Using multivariable Mendelian Randomization, we adjusted for potential pleiotropic or mediating effects relating to atrial fibrillation, coronary artery disease, and systolic blood pressure. Results: As expected, we observed strong independent associations between genetic predisposition to atrial fibrillation and cardioembolic stroke and between genetic predisposition to coronary artery disease as a proxy for atherosclerosis and large-artery stroke. Our data-driven analyses further indicated associations of genetic predisposition to both heart failure and lower resting heart rate with stroke. However, these associations were explained by atrial fibrillation, coronary artery disease, and systolic blood pressure in multivariable analyses. Genetically predicted P-wave terminal force in V1, an electrocardiographic marker for atrial cardiopathy, was inversely associated with large-artery stroke. Conclusions: Available genetic data do not support substantial effects of cardiac traits on the risk of stroke beyond known clinical risk factors. Our findings highlight the need to carefully control for confounding and other potential biases in studies examining candidate cardiac risk factors for stroke.

Mortality risk stratification in isolated severe traumatic brain injury using the revised cardiac risk index

Purpose Traumatic brain injury (TBI) continues to be a significant cause of mortality and morbidity worldwide. As cardiovascular events are among the most common extracranial causes of death after a severe TBI, the Revised Cardiac Risk Index (RCRI) could potentially aid in the risk stratification of this patient population. This investigation aimed to determine the association between the RCRI and in-hospital deaths among isolated severe TBI patients. Methods All adult patients registered in the TQIP database between 2013 and 2017 who suffered an isolated severe TBI, defined as a head AIS ≥ 3 with an AIS ≤ 1 in all other body regions, were included. Patients were excluded if they had a head AIS of 6. The association between different RCRI scores (0, 1, 2, 3, ≥ 4) and in-hospital mortality was analyzed using a Poisson regression model with robust standard errors while adjusting for potential confounders, with RCRI 0 as the reference. Results 259,399 patients met the study’s inclusion criteria. RCRI 2 was associated with a 6% increase in mortality risk [adjusted IRR (95% CI) 1.06 (1.01–1.12), p = 0.027], RCRI 3 was associated with a 17% increased risk of mortality [adjusted IRR (95% CI) 1.17 (1.05–1.31), p = 0.004], and RCRI ≥ 4 was associated with a 46% increased risk of in-hospital mortality [adjusted IRR(95% CI) 1.46 (1.11–1.90), p = 0.006], compared to RCRI 0. Conclusion An elevated RCRI ≥ 2 is significantly associated with an increased risk of in-hospital mortality among patients with an isolated severe traumatic brain injury. The simplicity and bedside applicability of the index makes it an attractive choice for risk stratification in this patient population.

Abstract 17059: Ocrelizumab Induced Kounis Syndrome

Kounis syndrome(KS), first described in 1991, is defined as concurrence of acute coronary syndrome and anaphylactic events. Primary mechanism of KS is interaction of mast cells with T-lymphocytes and macrophages via multidirectional stimuli leading to platelets activation. Case presentation: A 35 y.o. tennis coach with multiple sclerosis is admitted to the medical ICU with anaphylaxis after receiving Ocrelizumab infusion. Vital signs on presentation are significant for hypotension with blood pressure of 69/30 mm Hg, sinus tachycardia to 110 bpm and hypoxia with SatO2 88% on room air. Other investigations including chest x-ray, EKG and blood work are unrevealing for secondary pathological process outside of anaphylaxis. She undergoes fluid resuscitation followed by epinephrine drip for persistent hypotension. In addition methylprednisolone, famotidine and diphenhydramine are administered. She requires escalating doses of epinephrine and subsequently develops chest pain with troponin elevation to 0.29 ng/ml and EKG concerning for new ST depression and T wave inversion in II, III, aVF, V2 - V6 leads. Urgent echocardiography revealed normal biventricular function with no wall motion abnormalities and is only significant for moderate MR. Given excellent underlying functional capacity and no underlying cardiac risk factors, she was treated for Kounis syndrome by treating underlying anaphylaxis and weaning epinephrine as able with additional fluid resuscitation. Her chest pain resolved and EKG normalized with eventual discontinuation of epinephrine. Repeat echocardiography revealed preserved left ventricular (LV) function and mild MR. Discussion: KS is not a rare disease but easily overlooked and infrequently diagnosed. Our patient had the type I variant: endothelial dysfunction or microvascular angina in absence of cardiac risk factors. Inflammatory mediators can cause vasospasm and catecholamines used for treatment may potentiate it therefore requiring thoughtful dosing and appropriate duration of treatment. Prompt recognition is crucial for appropriate management of anaphylatic shock followed by that of ACS if LV function declines or risk factors for cardiac disease are present.