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To better understand the impact of Long COVID on an individual, we explored changes in daily wearable data (step count, resting heart rate (RHR), and sleep quantity) for up to one year in individuals relative to their pre-infection baseline among 279 people with and 274 without long COVID. Participants with Long COVID, defined as symptoms lasting for 30 days or longer, following a SARS-CoV-2 infection had significantly different RHR and activity trajectories than those who did not report Long COVID and were also more likely to be women, younger, unvaccinated, and report more acute-phase (first 2 weeks) symptoms than those without Long COVID. Demographic, vaccine, and acute-phase sensor data differences could be used for early identification of individuals most likely to develop Long COVID complications and track objective evidence of the therapeutic efficacy of any interventions. Trial Registration: https://classic.clinicaltrials.gov/ct2/show/NCT04336020. [ABSTRACT FROM AUTHOR]

Early identification of atrial fibrillation (AF) can reduce the risk of stroke, heart failure, and other serious cardiovascular outcomes. However, paroxysmal AF may not be detected even after a two-week continuous monitoring period. We developed a model to quantify the risk of near-term AF in a two-week period, based on AF-free ECG intervals of up to 24 h from 459,889 patch-based ambulatory single-lead ECG (modified lead II) recordings of up to 14 days. A deep learning model was used to integrate ECG morphology data with demographic and heart rhythm features toward AF prediction. Observing a 1-day AF-free ECG recording, the model with deep learning features produced the most accurate prediction of near-term AF with an area under the curve AUC = 0.80 (95% confidence interval, CI = 0.79–0.81), significantly improving discrimination compared to demographic metrics alone (AUC 0.67; CI = 0.66–0.68). Our model was able to predict incident AF over a two-week time frame with high discrimination, based on AF-free single-lead ECG recordings of various lengths. Application of the model may enable a digital strategy for improving diagnostic capture of AF by risk stratifying individuals with AF-negative ambulatory monitoring for prolonged or recurrent monitoring, potentially leading to more rapid initiation of treatment. [ABSTRACT FROM AUTHOR]

Digital health technologies will play an ever-increasing role in the future of healthcare. It is crucial that the people who will help make that transformation possible have the evidence-based and hands-on training necessary to address the many challenges ahead. To better prepare the future health workforce with the knowledge necessary to support the re-engineering of healthcare in an equitable, person-centric manner, we developed an experiential learning course—Wearables in Healthcare—for advanced undergraduate and graduate university students. Here we describe the components of that course and the lessons learned to help guide others interested in developing similar courses. [ABSTRACT FROM AUTHOR]

The ability to identify who does or does not experience the intended immune response following vaccination could be of great value in not only managing the global trajectory of COVID-19 but also helping guide future vaccine development. Vaccine reactogenicity can potentially lead to detectable physiologic changes, thus we postulated that we could detect an individual's initial physiologic response to a vaccine by tracking changes relative to their pre-vaccine baseline using consumer wearable devices. We explored this possibility using a smartphone app-based research platform that enabled volunteers (39,701 individuals) to share their smartwatch data, as well as self-report, when appropriate, any symptoms, COVID-19 test results, and vaccination information. Of 7728 individuals who reported at least one vaccination dose, 7298 received an mRNA vaccine, and 5674 provided adequate data from the peri-vaccine period for analysis. We found that in most individuals, resting heart rate (RHR) increased with respect to their individual baseline after vaccination, peaked on day 2, and returned to normal by day 6. This increase in RHR was greater than one standard deviation above individuals' normal daily pattern in 47% of participants after their second vaccine dose. Consistent with other reports of subjective reactogenicity following vaccination, we measured a significantly stronger effect after the second dose relative to the first, except those who previously tested positive to COVID-19, and a more pronounced increase for individuals who received the Moderna vaccine. Females, after the first dose only, and those aged <40 years, also experienced a greater objective response after adjusting for possible confounding factors. These early findings show that it is possible to detect subtle, but important changes from an individual's normal as objective evidence of reactogenicity, which, with further work, could prove useful as a surrogate for vaccine-induced immune response. [ABSTRACT FROM AUTHOR]

Individual smartwatch or fitness band sensor data in the setting of COVID-19 has shown promise to identify symptomatic and pre-symptomatic infection or the need for hospitalization, correlations between peripheral temperature and self-reported fever, and an association between changes in heart-rate-variability and infection. In our study, a total of 38,911 individuals (61% female, 15% over 65) have been enrolled between March 25, 2020 and April 3, 2021, with 1118 reported testing positive and 7032 negative for COVID-19 by nasopharyngeal PCR swab test. We propose an explainable gradient boosting prediction model based on decision trees for the detection of COVID-19 infection that can adapt to the absence of self-reported symptoms and to the available sensor data, and that can explain the importance of each feature and the post-test-behavior for the individuals. We tested it in a cohort of symptomatic individuals who exhibited an AUC of 0.83 [0.81–0.85], or AUC = 0.78 [0.75–0.80] when considering only data before the test date, outperforming state-of-the-art algorithm in these conditions. The analysis of all individuals (including asymptomatic and pre-symptomatic) when self-reported symptoms were excluded provided an AUC of 0.78 [0.76–0.79], or AUC of 0.70 [0.69–0.72] when considering only data before the test date. Extending the use of predictive algorithms for detection of COVID-19 infection based only on passively monitored data from any device, we showed that it is possible to scale up this platform and apply the algorithm in other settings where self-reported symptoms can not be collected. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic has accelerated the adoption of innovative healthcare methods, including remote patient monitoring. In the setting of limited healthcare resources, outpatient management of individuals newly diagnosed with COVID-19 was commonly implemented, some taking advantage of various personal health technologies, but only rarely using a multi-parameter chest-patch for continuous monitoring. Here we describe the development and validation of a COVID-19 decompensation index (CDI) model based on chest patch-derived continuous sensor data to predict COVID-19 hospitalizations in outpatient-managed COVID-19 positive individuals, achieving an overall AUC of the ROC Curve of 0.84 on 308 event negative participants, and 22 event positive participants, out of an overall study cohort of 400 participants. We retrospectively compare the performance of CDI to standard of care modalities, finding that the machine learning model outperforms the standard of care modalities in terms of both numbers of events identified and with a lower false alarm rate. While only a pilot phase study, the CDI represents a promising application of machine learning within a continuous remote patient monitoring system. [ABSTRACT FROM AUTHOR]

Background: AWAKE-HF evaluated the effect of the initiation of sacubitril/valsartan versus enalapril on activity and sleep using actigraphy in patients who have heart failure with reduced ejection fraction (HFrEF). Methods: In this randomized, double-blind study, patients with HFrEF (n = 140) were randomly assigned to sacubitril/valsartan or enalapril for 8 weeks, followed by an 8-week open-label phase with sacubitril/valsartan. Primary endpoint was change from baseline in mean activity counts during the most active 30 min/day at week 8. The key secondary endpoint was change in mean nightly activity counts/minute from baseline to week 8. Kansas City Cardiomyopathy Questionnaire-23 (KCCQ-23) was an exploratory endpoint. Results: There were no detectable differences between groups in geometric mean ratio of activity counts during the most active 30 min/day at week 8 compared with baseline (0.9456 [sacubitril/valsartan:enalapril]; 95% confidence interval [CI] 0.8863–1.0088; P = 0.0895) or in mean change from baseline in activity during sleep (difference: 2.038 counts/min; 95% CI − 0.062 to 4.138; P = 0.0570). Change from baseline to week 8 in KCCQ-23 was 2.89 for sacubitril/valsartan and 4.19 for enalapril, both nonsignificant. Conclusions: In AWAKE-HF, no detectable differences in activity and sleep were observed when comparing sacubitril/valsartan with enalapril in patients with HFrEF using a wearable biosensor. Clinical trial registration: ClinicalTrials.gov, NCT02970669. [ABSTRACT FROM AUTHOR]

In platelets, thrombin receptor signaling depends upon the release of adenosine diphosphate and subsequent activation at purinergic subtype Y (P2Y) receptors. The purpose of this study is to evaluate the influence of specific P2Y polymorphisms on platelet reactivity in healthy subjects mediated by thrombin receptor activating peptide (TRAP). We recruited a total of 29 healthy volunteers who had been previously genotyped for two polymorphisms of the P2Y receptor: the H2 haplotype (rs2046934) and 34C>T (rs6785930). Flow cytometry and the VerifyNow assay were used to assess platelet activation and aggregation stimulated by TRAP in the presence and absence of specific receptor antagonists for the P2Y, P2Y, and thromboxane A2 receptors. We identified a significant recessive effect of the P2Y-receptor H2 haplotype on TRAP-induced flow cytometry. Specifically, H2/H2 carriers ( n = 5) demonstrated a significant reduction in both glycoprotein IIb/IIIa receptor activation ( p < 0.001) and CD62P expression ( p = 0.035). While the VerifyNow assay did not reveal any effect of haplotype on TRAP-mediated platelet aggregation ( p = 0.72), the H2/H2 subjects demonstrated greater platelet inhibition in the presence of cangrelor, a specific receptor antagonist for the P2Y receptor ( p = 0.023). No consistent effects of the separate 34C>T genotype (rs6785930) were demonstrated under the conditions evaluated. The findings of this study suggest a potential association between P2Y-receptor H2/H2 carriers and reduced platelet function mediated by TRAP in healthy volunteers. [ABSTRACT FROM AUTHOR]

The contribution of platelets in the pathophysiology of low-shear thrombosis-specifically, in atrial fibrillation (AF) and venous thromboembolic events (VTE)-remains less clear than for arterial thrombosis. AF itself appears to lead to platelet activation, offering a potential target for aspirin and other antiplatelet agents. Randomized trial results suggest a small benefit of aspirin over placebo, and of dual antiplatelet therapy (aspirin plus clopidogrel) over aspirin alone, for prevention of cardioembolic events in AF. Antiplatelet therapy thus can represent an option for patients with AF who are unsuitable for therapy with warfarin or novel oral anticoagulant agents. For VTE, the rationale for antiplatelet therapy reflects the venous response to disrupted blood flow-interactions among monocytes, neutrophil extracellular traps, and platelets. Early randomized trials generally showed poorer performance of aspirin relative to heparins and danaparoid sodium in prevention of VTE. However, results from large placebo- and dalteparin-controlled randomized trials have spurred changes in the most recent practice guidelines-aspirin is now recommended after major orthopedic surgery for patients who cannot receive other antithrombotic therapies. [ABSTRACT FROM AUTHOR]

Improving quality of care through the enhanced use of digital technologies is becoming an increasingly primary focus of the health care industry in general and cardiovascular (CV) medicine in particular. The recent rapid adoption of electronic health records (EHR) has the potential to improve the management of CV disease by removing variability and assuring at least consideration of guideline-recommended care and appropriate use criteria. This can lead to improved cardiac outcomes at all phases of care; beginning with the automated identification of patients who are at increased risk, implementing evidence based medicine for primary CV prevention, using online decision support tools for acute management, and, possibly most importantly, by connecting the health care provider and the patient through open accessibility to their EHR. The widespread use of EHR is the dawn of a new era where evidence based guidelines can be seamlessly translated to patient care and where patients are actively involved in their own health. As transformative as this will be, it is important to recognize that we are currently experiencing only the very earliest potential of the EHR in improving CV outcomes. [ABSTRACT FROM AUTHOR]

Clopidogrel use prior to coronary artery bypass graft surgery in patients presenting with acute coronary syndromes is associated with a greater incidence of procedural related morbidity. We studied the impact of clopidogrel pre-treatment in patients undergoing off-pump versus on-pump coronary revascularization. This report describes a post hoc analysis of 431 on-pump and 165 off-pump cases from a retrospective multicenter study of the impact of preoperative (within 5 days) clopidogrel use on bleeding related outcomes and surgical reintervention. Logistic regression was used to analyze the outcomes with respect to surgery type and clopidogrel exposure while using a propensity score risk adjustment for off-pump surgery. The hospital length of stay (9.3 ± 5.4 days vs. 8.9 ± 5.3 days, p = 0.35), major bleeding (21% vs. 20%, p = 0.74) and reoperation (3.7% vs. 4.8%, p = 0.53) were similar between on-pump and off-pump, respectively. In both surgical cohorts, recent clopidogrel use was associated with a greater incidence of major bleeding, reoperation, and transfusion. After multivariable adjustment, the odds ratio of major bleeding (1.76, 95% confidence interval 0.88-3.52 on-pump; 2.37, 95% confidence interval 1.06-5.30 off-pump) and reoperation (4.52, 95% confidence interval 0.58-36.6 in on-pump; 7.05, 95% confidence interval 0.82-60.5 in off-pump) was increased in clopidogrel-treated patients compared to no clopidogrel. Major bleeding and reoperation did not differ significantly between patients undergoing on- or off-pump surgery. Clopidogrel treatment within 5 days prior to surgery increased the risk of bleeding and reoperation in all CABG patients irrespective of whether surgery was performed on- or off-pump. [ABSTRACT FROM AUTHOR]

Bleeding events have been associated with adverse early and late outcomes in virtually all clinical settings. The mechanism behind this observation remains poorly understood. We sought to determine if the reason might be the provocation of an inflammatory response by bleeding events. In a formal substudy of the ACUITY trial, plasma samples of a range of biomarkers were collected at baseline, discharge, 30 days, and 1 year from 192 patients with acute coronary syndromes (ACS) and were analyzed in a central core laboratory. Temporal changes in biomarker levels were assessed in patients who experienced in-hospital hemorrhagic events, recurrent ischemic events, or neither. Sixteen patients were excluded from the study (7 with incomplete samples, 5 undergoing coronary artery bypass grafting (CABG) during index hospitalization; 1 had both bleeding and ischemic events). Median high sensitivity C-reactive protein (hs-CRP) levels (mg/l) increased significantly more from admission to discharge among the 9 patients who experienced an in-hospital major bleed compared to either the 9 patients who had a recurrent ischemic event (+6.0 vs. +0.70, P = 0.04) or the 151 patients who had no event (+6.0 vs. +0.60, P = 0.003). Compared to patients with no in-hospital events, median interleukin-6 (IL-6) levels (pg/ml) increased from admission to hospital discharge non-significantly in those with a bleeding event (+0.92 vs. +2.46, P = 0.55) and in those who experienced an in-hospital recurrent ischemic event (+0.92 vs. +3.60, P = 0.09). These data suggest that major bleeding is associated with development of a pro-inflammatory state. If confirmed, this mechanism may in part explain the poor prognosis of patients experiencing an acute hemorrhagic event. [ABSTRACT FROM AUTHOR]

This article focuses on lessons learned from clinical trials of antiplatelet therapies—in particular, that the degree of inhibition of ex vivo platelet aggregation does not necessarily directly translate into clinical efficacy. As an example, the case of the oral platelet glycoprotein IIb/IIIa inhibitors is presented, in which despite consistent evidence of substantial inhibition of platelet aggregation, this class of drugs provided no clinical benefit in Phase III trials and, in fact, was harmful. Several hypotheses for these unexpected findings have been proposed, but none has been confirmed. The connection between ex vivo inhibition of platelet aggregation and clinical benefit of platelet P2Y12 antagonists is also not straightforward and is currently being tested in large clinical trials. A link between inflammatory status and clinical benefit from antiplatelet agents continues to emerge and highlights the fact that biomarkers beyond ex vivo platelet aggregation may predict the clinical benefit of antiplatelet agents that can reduce platelet activation (i.e., aspirin and thienopyridines). Results of past and ongoing trials hold valuable clues to determining the appropriate targets for maximizing antiplatelet efficacy, but the current lack of a proven ex vivo assay that correlates with clinical outcomes hampers clinical investigation, drug development programs, and clinical practice. [ABSTRACT FROM AUTHOR]

Atherothrombosis is the common link between clinical manifestations of arterial vascular disease including ischemic stroke and acute coronary syndromes, such as unstable angina and acute myocardial infarction. Our understanding of the common pathologic mechanisms underlying these conditions has significantly increased during the past ten years, yet atherothrombosis as the "root cause" of a large proportion of cardiovascular and cerebrovascular diseases is largely underappreciated. Although the classical risk factors of dyslipidemia, smoking, diabetes, hypertension, obesity, and sedentary lifestyle are widely recognized as being associated with a heightened risk of vascular disease, inflammation of the vascular system during the past decade has become increasingly regarded as the principal underlying mechanism in the development of clinical atherothrombotic disease. In addition, platelet-derived inflammatory mediators play an essential role in the pathogenesis of cardiovascular disease, being involved at all stages of plaque development until their eventual rupture and subsequent formation of a platelet-rich thrombus. Mounting evidence supports the role of both localized and systemic inflammation in these events. Platelets are central to vascular inflammatory processes. Thus, inflammation can stimulate local thrombosis and thrombosis can amplify inflammation. Consequently, antiplatelet therapy for the prevention of serious vascular events may provide a double benefit via an anti-inflammatory action of the antiplatelet agent in modifying plaque formation and stability and antiplatelet activity that inhibits platelet aggregation and thrombus formation from occurring following plaque rupture. [ABSTRACT FROM AUTHOR]

Platelet adhesion, activation, and aggregation at sites of vascular endothelial disruption caused by atherosclerosis are key events in arterial thrombus formation. Platelet tethering and adhesion to the arterial wall, particularly under high shear forces, are achieved through multiple high-affinity interactions between platelet membrane receptors (integrins) and ligands within the exposed subendothelium, most notably collagen and von Willebrand factor (vWF). Platelet adhesion to collagen occurs both indirectly, via binding of the platelet glycoprotein (GP) Ib-V-IX receptor to circulating vWF, which binds to exposed collagen, and directly, via interaction with the platelet receptors GP VI and GP Ia/IIb. Platelet activation, initiated by exposed collagen and locally generated soluble platelet agonists (primarily thrombin, ADP, and thromboxane A2), provides the stimulus for the release of platelet-derived growth factors, adhesion molecules and coagulation factors, activation of adjacent platelets, and conformational changes in the platelet αIIbβ3 integrin (GP IIb/IIIa receptor). Platelet aggregation, mediated primarily by interaction between the activated platelet GP IIb/IIIa receptor and its ligands, fibrinogen and vWF, results in the formation of a platelet-rich thrombus. Currently available antiplatelet drugs (aspirin [acetylsalicylic acid], dipyridamole, clopidogrel, ticlopidine, abciximab, eptifibatide, tirofiban) act on specific targets to inhibit platelet activation and aggregation. Elucidation of the multiple mechanisms involved in platelet thrombus formation provides opportunities for selectively inhibiting the pathways most relevant to the pathophysiology of atherothrombosis. [ABSTRACT FROM AUTHOR]

Background: Increased platelet reactivity can identify patients at high risk for thrombotic events, but its clinical use has been impractical due to technical limitations. The purpose of the present study is to determine if a point-of-care measurement of platelet function in patients presenting to an emergency room with chest pain can identify those at high risk of adverse cardiac events. Methods: Platelet function was measured using the Ultegra-RPFA in 201 patients presenting to the emergency department with the primary complaint of chest pain and either known coronary disease or at least one cardiac risk factor. The primary endpoint was any major adverse cardiac events (MACE) [cardiac death, myocardial infarction (MI), re-admission for coronary revascularization] 6 months post-enrollment. Results: Platelet function at baseline ranged from 44 to 315 platelet activation units (PAU) (mean 175 ± 6). Seventy-six patients experienced MACE (37.8%) by 6 months post-enrollment. Mean PAU was significantly lower in the group experiencing MACE (166 ± 9 vs. 181 ± 9; p = 0.026). By univariate analysis, admission PAU was a significant predictor of MACE at 6 months ( p = 0.028). However, when adjusted for age, gender, cardiac risk factors, and a history of coronary artery disease (CAD) using multivariate logistic regression analysis, PAU was no longer significantly predictive of MACE ( p = 0.268). Conclusions: Point-of-care testing of platelet function deserves further study for risk assessment and individualized therapy in the future. Abbreviated Abstract. Platelet function was assessed in 201 patients presenting to the emergency department with chest pain using a point-of-care device to measure platelet activation, the Ultegra-RPFA. Platelet function, expressed in platelet activation units (PAU), was significantly lower in patients who experienced adverse cardiac events ( p = 0.026). By univariate analysis, PAU was a significant predictor of cardiac death, MI, and re-hospitalization for revascularization at 6 months ( p = 0.028). However, when adjusted for age, gender, cardiac risk factors, and coronary artery disease (CAD), PAU was no longer significantly predictive of the above combined endpoint ( p = 0.268). [ABSTRACT FROM AUTHOR]

Until recently, long-term antiplatelet therapy for the treatment and prevention of the complications of atherothrombotic disease was limited to aspirin. Although an incredibly costeffective therapy, in placebo-controlled clinical trials approximately 75% of patients at risk continue to experience thrombotic events despite chronic aspirin therapy. The availability of the thienopyridines, in particular clopidogrel, represents an important addition to the physician’s armamentarium. A number of clinical trials have confirmed the efficacy of the combination of clopidogrel and aspirin therapy compared with aspirin alone, with multiple other important largescale clinical trials currently ongoing. The exact mechanism of this benefit is still being elucidated but is clearly related to the inhibition of the many consequences of platelet activation—vascular inflammation, endothelial dysfunction, and localized angiogenesis/mitogenesis—and not just aggregation. [ABSTRACT FROM AUTHOR]

Over the past two decades, we have witnessed a large decrease in the death and complication rate of patients experiencing acute myocardial infarction (MI), due to our ability to restore blood flow to infarct-related arteries. Therapies include strategies to inhibit platelet function and induce fibrinolysis, and mechanical reperfusion with percutaneous intervention. Despite decreases in morbidity and mortality with thrombolytic therapy, reperfusion rates remain less than optimal. With standard fibrinolytic therapy in combination with aspirin, it is thought that thrombolyticinduced platelet activation may be an important reason for failure to induce perfusion, or maintain reperfusion in the infarct-related artery. In the past 10 years we have moved from platelet inhibition with aspirin to newer, more potent platelet inhibitors such as glycoprotein (GP) IIb/IIIa antagonists. Recent trials have evaluated the efficacy and safety of combining thrombolytic drugs with GP IIb/IIIa receptor antagonists. Future trends may use combination therapy as a part of a mechanical strategy, using these medications to induce early reperfusion as the patient is prepared for percutaneous intervention. This review summarizes recently published trials using combination thrombolytic and GP IIb/ IIIa receptor inhibitor therapy in the treatment of acute MI. [ABSTRACT FROM AUTHOR]

One by-product of the flurry of large-scale clinical trials accompanying the emergence of drugs that inhibit platelet function is volumes of information chronicling the adverse effects of this class of medications. One aspect all antiplatelet drugs share is a propensity toward bleeding. Beyond that similarity, however, the different pharmacologic agents in this broad collection have few attributes in common. Aspirin, by virtue of its long history, has been studied most extensively, and has proven to be an exceptionally valuable therapy. However, the complicated adverse profile of this seemingly simple drug is commonly overlooked by practitioners and deserves clinical review. The thienopyridine class (including ticlopidine and clopidogrel) share certain peculiarities that continue to be clarified, including life-threatening thrombotic thrombocytopenia purpura. Dipyridamole is a veteran drug that is enjoying renewed attention as a prophylactic aid in preventing cerebrovascular events. One class, the oral platelet glycoprotein IIb/IIIa receptor inhibitors, has failed to find its way into clinical implementation due to an unfavorable balance between efficacy and adverse effect. This review summarizes the adverse profiles of each of these drug classes and draws on data gathered in large clinical studies. [ABSTRACT FROM AUTHOR]

Today, following coronary stenting, clopidogrel has largely replaced ticlopidine as part of combination antiplatelet therapy following coronary stenting primarily due to its better tolerability. While there is no randomized, blinded, efficacy trial of ticlopidine versus clopidogrel, there are ample data from a number of observational studies, randomized non-blinded trials, and a randomized blinded safety trial to prove that clopidogrel is not only safer than ticlopidine, but also at least as efficacious following stenting. With over 10,000 treated patients, pooled data suggest similar rates of stent thrombosis (clopidogrel 0.98% vs. ticlopidine 0.98%) and lower rates of major adverse cardiac events with clopidogrel (clopidogrel 1.63% vs. ticlopidine 4.52%, p<0.001), with a clear advantage for clopidogrel regarding adverse events (clopidogrel 5.91% vs. ticlopidine 9.75%, p<0.001). With clopidogrel's superior safety and at least equivalent efficacy, the question of “which thienopyridine?” post-stenting has been answered. Now the questions “how much?”, “how soon?” and “how long?” must be addressed. The Clopidogrel for the Reduction of Events During Observation (CREDO) trial is a multi-center, double-blind, randomized trial designed to answer these remaining questions. CREDO will evaluate the efficacy and safety of clopidogrel pretreatment versus no pretreatment, and prolonged (1 year), versus short-term (1 month) dual antiplatelet therapy in 2,000 patients undergoing planned or highly probable coronary intervention with a stent. [ABSTRACT FROM AUTHOR]

Purpose of the review: Advances in computing power and wireless technologies have reshaped our approach to patient monitoring. Medical grade sensors and apps that were once restricted to hospitals and specialized clinic are now widely available. Here, we review the current evidence supporting the use of connected health technologies for the prevention and management of cardiovascular disease in an effort to highlight gaps and future opportunities for innovation. Recent findings: Initial studies in connected health for cardiovascular disease prevention and management focused primarily on activity tracking and blood pressure monitoring but have since expanded to include a full panoply of novel sensors and pioneering smartphone apps with targeted interventions in diet, lipid management and risk assessment, smoking cessation, cardiac rehabilitation, heart failure, and arrhythmias. While outfitting patients with sensors and devices alone is infrequently a lasting solution, monitoring programs that include personalized insights based on patient-level data are more likely to lead to improved outcomes. Advances in this space have been driven by patients and researchers while healthcare systems remain slow to fully integrate and adequately adapt these new technologies into their workflows. Summary: Cardiovascular disease prevention and management continue to be key focus areas for clinicians and researchers in the connected health space. Exciting progress has been made though studies continue to suffer from small sample size and limited follow-up. Efforts that combine home patient monitoring, engagement, and personalized feedback are the most promising. Ultimately, combining patient-level ambulatory sensor data, electronic health records, and genomics using machine learning analytics will bring precision medicine closer to reality. [ABSTRACT FROM AUTHOR]

Ramipril is an oral, non-sulfhydryl ACE inhibitor thought to act in the renin-angiotensin-aldosterone system to decrease vasopressor activity, aldosterone secretion, and bradykinin degradation.Ramipril is generally well tolerated and effective in the treatment of patients aged ≥55 years at high risk for the development of cardiovascular (CV) events, in whom the risk of myocardial infarction (MI), stroke, and CV death can be significantly reduced. The risk of these CV outcomes may also be reduced with ramipril therapy in various subgroups; these include patients with diabetes mellitus, peripheral arterial disease (PAD) or renal insufficiency, and women. Thus, ramipril, in addition to lifestyle interventions, should be considered an important therapy in the prevention of CV outcomes in high-risk patients. [ABSTRACT FROM AUTHOR]