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Urban environments contribute substantially to the rising burden of cardiometabolic diseases worldwide. Cities are complex adaptive systems that continually exchange resources, shaping exposures relevant to human health such as air pollution, noise, and chemical exposures. In addition, urban infrastructure and provisioning systems influence multiple domains of health risk, including behaviors, psychological stress, pollution, and nutrition through various pathways (eg, physical inactivity, air pollution, noise, heat stress, food systems, the availability of green space, and contaminant exposures). Beyond cardiometabolic health, city design may also affect climate change through energy and material consumption that share many of the same drivers with cardiometabolic diseases. Integrated spatial planning focusing on developing sustainable compact cities could simultaneously create heart-healthy and environmentally healthy city designs. This article reviews current evidence on the associations between the urban exposome (totality of exposures a person experiences, including environmental, occupational, lifestyle, social, and psychological factors) and cardiometabolic diseases within a systems science framework, and examines urban planning principles (eg, connectivity, density, diversity of land use, destination accessibility, and distance to transit). We highlight critical knowledge gaps regarding built-environment feature thresholds for optimizing cardiometabolic health outcomes. Last, we discuss emerging models and metrics to align urban development with the dual goals of mitigating cardiometabolic diseases while reducing climate change through cross-sector collaboration, governance, and community engagement. This review demonstrates that cities represent crucial settings for implementing policies and interventions to simultaneously tackle the global epidemics of cardiovascular disease and climate change.

The paper discusses the relationship between non-optimal temperature and cardiovascular disease (CVD) and presents the first-to-date quantification of the global temperature-related CVD burden. Key findings include: Non-optimal temperatures were responsible for a significant proportion of global cardiovascular deaths between 1990 and 2019.People in lower socioeconomic regions were more vulnerable to the effects of non-optimal temperature on CVD than those in higher socioeconomic regions.

In this review, sex, racial, and ethnic differences in acute coronary syndromes on a global scale are summarized. The relationship between disparities in presentation and management of acute coronary syndromes and effect on worse clinical outcomes in acute coronary syndromes are discussed. The effect of demographic, geographic, racial, and ethnic factors on acute coronary syndrome care disparities are reviewed. Differences in risk factors including systemic inflammatory disorders and pregnancy-related factors and the pathophysiology underlying them are discussed. Finally, breast arterial calcification and coronary calcium scoring are discussed as methods to detect subclinical atherosclerosis and start early treatment in an attempt to prevent clinical disease.

BackgroundHot, desert Gulf countries are host to millions of migrant workers doing outdoor jobs such as construction and hospitality. The Gulf countries apply a summertime ban on midday work to protect workers from extreme heat, although without clear evidence of effectiveness. We assessed the risk of occupational injuries associated with extreme hot temperatures during the summertime ban on midday work in Kuwait.MethodsWe collected daily occupational injuries in the summer months that are reported to the Ministry of Health’s Occupational Health Department for 5 years from 2015 to 2019. We fitted generalised additive models with a quasi-Poisson distribution in a time series design. A 7-day moving average of daily temperature was modelled with penalised splines adjusted for relative humidity, time trend and day of the week.ResultsDuring the summertime ban, the daily average temperature was 39.4°C (±1.8°C). There were 7.2, 7.6 and 9.4 reported injuries per day in the summer months of June, July and August, respectively. Compared with the 10th percentile of summer temperatures in Kuwait (37.0°C), the average day with a temperature of 39.4°C increased the relative risk of injury to 1.44 (95% CI 1.34 to 1.53). Similarly, temperatures of 40°C and 41°C were associated with relative risks of 1.48 (95% CI 1.39 to 1.59) and 1.44 (95% CI 1.27 to 1.63), respectively. At the 90th percentile (42°C), the risks levelled off (relative risk 1.21; 95% CI 0.93 to 1.57).ConclusionWe found substantial increases in the risk of occupational injury from extremely hot temperatures despite the ban on midday work policy in Kuwait. ‘Calendar-based’ regulations may be inadequate to provide occupational heat protections, especially for migrant workers.

Climate change is the greatest existential challenge to planetary and human health and is dictated by a shift in the Earth’s weather and air conditions owing to anthropogenic activity. Climate change has resulted not only in extreme temperatures, but also in an increase in the frequency of droughts, wildfires, dust storms, coastal flooding, storm surges and hurricanes, as well as multiple compound and cascading events. The interactions between climate change and health outcomes are diverse and complex and include several exposure pathways that might promote the development of non-communicable diseases such as cardiovascular disease. A collaborative approach is needed to solve this climate crisis, whereby medical professionals, scientific researchers, public health officials and policymakers should work together to mitigate and limit the consequences of global warming. In this Review, we aim to provide an overview of the consequences of climate change on cardiovascular health, which result from direct exposure pathways, such as shifts in ambient temperature, air pollution, forest fires, desert (dust and sand) storms and extreme weather events. We also describe the populations that are most susceptible to the health effects caused by climate change and propose potential mitigation strategies, with an emphasis on collaboration at the scientific, governmental and policy levels.

Limited data exist on the risk profile and outcomes among young patients with acute myocardial infarction(AMI) in low-and middle-income countries(LMICs). This study explored differences in the clinical characteristics, medical care, and outcomes of AMI in young adults in India with a subanalysis focusing on sex disparities amongst the young.

IMPORTANCE: Visit-to-visit blood pressure variability (BPV) is associated with cardiovascular events, but mechanisms and therapeutic implications underlying this association are not well understood. OBJECTIVE: To examine the association of intraindividual BPV, coronary atheroma progression, and clinical outcomes using serial intravascular ultrasonography. DESIGN, SETTING, AND PARTICIPANTS: Post hoc patient-level analysis of 7 randomized clinical trials conducted from 2004 to 2016 involving 3912 patients in multicenter, international, clinic-based primary and tertiary care centers. Adult patients with coronary artery disease who underwent serial intravascular ultrasonography in the setting of a range of medical therapies were included. Data were analyzed between November 2017 and March 2019. EXPOSURES: Visit-to-visit BPV measured using intraindividual standard deviation over 3, 6, 12, 18, and 24 months. MAIN OUTCOMES AND MEASURES: Percent atheroma volume (PAV) progression and major adverse cardiovascular events (defined as death, myocardial infarction, stroke, urgent revascularization for acute coronary syndrome, and hospitalization for unstable angina). RESULTS: Of 3912 patients, the mean (SD) age was 58 (9) years, 1093 (28%) were women, and 3633 (93%) were white . Continuous change in PAV was significantly associated with systolic BPV (β, .049; 95% CI, 0.021-0.078; P = .001), diastolic BPV (β, .031; 95% CI, 0.002-0.059; P = .03), and pulse pressure variability (β, .036; 95% CI, 0.006-0.067; P = .02), without a signal for differential effect greater than or less than a mean BP of 140/90 mm Hg. The PAV progression as a binary outcome was significantly associated with systolic BPV (odds ratio, 1.09; 95% CI, 1.01-1.17; P = .02) but not diastolic BPV (odds ratio, 1.04; 95% CI, 0.97-1.11; P = .30) or pulse pressure variability (odds ratio, 1.03; 95% CI, 0.96-1.10; P = .47). Survival curves revealed a significant stepwise association between cumulative major adverse cardiovascular events and increasing quartiles of systolic BPV (Kaplan-Meier estimates for quartiles 1-4: 6.1% vs 8.5% vs 10.1% vs 12.0%, respectively; log-rank P <.001). These distinct stepwise associations were not seen with diastolic BPV or pulse pressure variability. CONCLUSIONS AND RELEVANCE: Greater BPV, particularly systolic BPV, is significantly associated with coronary atheroma progression and adverse clinical outcomes. These data suggest maintaining stable blood pressure levels may be important to further improve outcomes in patients with coronary disease.

Globally, more people die from cardiovascular disease than any other cause. Climate change, through amplified environmental exposures, will promote and contribute to many noncommunicable diseases, including cardiovascular disease. Air pollution, too, is responsible for millions of deaths from cardiovascular disease each year. Although they may appear to be independent, interchangeable relationships and bidirectional cause-and-effect arrows between climate change and air pollution can eventually lead to poor cardiovascular health. In this topical review, we show that climate change and air pollution worsen each other, leading to several ecosystem-mediated effects. We highlight how increases in hot climates as a result of climate change have increased the risk of major air pollution events such as severe wildfires and dust storms. In addition, we show how altered atmospheric chemistry and changing patterns of weather conditions can promote the formation and accumulation of air pollutants: a phenomenon known as the climate penalty. We demonstrate these amplified environmental exposures and their associations to adverse cardiovascular health outcomes. The community of health professionals—and cardiologists, in particular—cannot afford to overlook the risks that climate change and air pollution bring to the public’s health.

Background:Liraglutide, a GLP-1- receptor agonists approved for the treatment of type 2 diabetes and obesity confers a lower CVD mortality. However, mechanisms underlying this finding remain unknown, particularly in normoglycemic subjects. We investigated the effects of liraglutide on the progression and pathobiology of atherosclerosis using multimodal intravascular imaging in rabbits.Methods:Rabbits atherosclerosis (N=16) were induced by balloon injury of the abdominal aorta and cholesterol feeding for 6 weeks. Then, rabbits were imaged with intravascular ultrasound (IVUS) and near-infrared fluorescence optical coherence tomography (NIRF-OCT) for the analysis of plaque burden and plaque inflammation (ProSense VM110 NIRF agent, 4 mg/kg/iv) respectively. Next, rabbits were randomized into: Control (n=8) or liraglutide (n=8, 0.1 mg/kg/day) groups. Imaging was repeated after 4 weeks, followed by histopathology and RNA analysis. On per-slice basis (every 0.4 mm) of IVUS imaging, the percent atheroma volume (PAV) was measured across the 40 mm balloon injured area. Atheroma progression was quantified as the ΔPAV between 6 and 10 weeks.Results:IVUS analyses (3200 slices/16 rabbits) revealed that liraglutide significantly reduced plaque progression (ΔPAV, 1.5% [0.2-2.8] vs. 9.3% [6.7-13.0] control, p=0.05). In vivo distance-corrected VM110 cathepsin inflammatory plaque activity was similar (ΔNIRF average plaque 25.2 [-9.8- 62] vs. 22.6 [3.9- 52.5] nM control, p=0.72). Plaques from liraglutide-treated animals however exhibited fewer RAM11+ macrophages (21.3±11.4 vs. control 30.9±16.7 macrophages/section, p=0.01) stry. Both plaques showed similar αSMA (45.2±6.7% vs 52.4±1.2% αSMA+ area/section, p=0.327). Liraglutide decreased inflammatory RNA transcripts (IL-6 and TNF-α), and RNA-seq transcriptomic analysis revealed that liraglutide altered inflammatory and metabolic pathways (as CRP, CYP3A6, Apo-A4 and FMO3). Blood glucose was normal and similar between groups (p>0.05).Conclusion:Liraglutide suppresses in vivo atherosclerotic plaque progression and plaque macrophage expression in normoglycemic rabbits. Further investigation of its plaque stabilizing effects in subjects with and without diabetes is warranted.

Introduction:Patients with diabetes are more likely to experience an acute myocardial infarction (AMI), heart failure, or death from cardiovascular (CV) causes than patients without diabetes. Despite cardiovascular disease being the leading cause of death in India, limited data exists on the outcome of patients with diabetes who suffer acute cardiovascular events.Hypothesis:Diabetes is common in patients with acute myocardial infarction (AMI) in India and is associated with worse in-hospital and 30-day cardiovascular outcomes.Methods:We examined 21374 patients with AMI enrolled in the Acute Coronary Syndrome Quality Improvement in Kerala trial. We compared those with and without diabetes with regards to the development of in-hospital and 30-day major adverse cardiac events including death, re-infarction, stroke, or major bleeding. The associations between diabetes and cardiac outcomes were adjusted for presentation and in-hospital management using logistic regression.Results:mean±SD age was 60.1±12.0 years and 24.3% were females. A total of 44.4% of AMI patients had diabetes. Those with diabetes were more likely to be older, female, with hypertension and have higher Killip class on presentation but less likely to present with STEMI. Patients with diabetes had longer symptoms onset-to-arrival (median 225 vs 290 min; P<0.001) and, in case of STEMI, longer door-to-balloon times (median, 75.0 vs 91 min; P<0.001). Diabetes was independently associated with higher in-hospital death (adjusted odds ratio [aOR], 1.46; 95% CI, 1.12-1.89), in-hospital reinfarction (aOR 1.52; 95% CI, 1.15-2.02). Diabetes was also associated with higher 30-day MACE (aOR, 1.33; 95% CI, 1.14-1.55) and 30-day death (aOR, 1.40; 95%CI, 1.16-1.69) but not 30-day stroke or 30-day bleeding.Conclusion:Among patients presenting with AMI in Kerala, India, a considerable proportion has diabetes and are at increased risk for in-hospital and 30-day adverse cardiovascular outcomes. Increased awareness of the increased CV risk and attention to the implementation of established cardiovascular therapies are indicated for patients with diabetes in lower-middle income countries who develop AMI.

Introduction:A pharmacoinvasive reperfusion strategy is recommended for ST-elevation myocardial infarction (STEMI) patients when primary percutaneous coronary intervention (PCI) cannot be achieved in a timely fashion. This is based on a limited number of trials. The effectiveness of this strategy in the real-world setting is debatable.Hypothesis:Pharmacoinvasive strategy has comparable outcome to primary PCI, when PCI is not readily available. This project was part of improving STEMI network in Kuwait.Methods:The use of reperfusion in ST-elevation myocardial infarction in Kuwait (REPERFUSE Kuwait) is a prospective, multicenter, cohort-based registry of all patients who presented with acute ST-segment elevation myocardial infarction (STEMI) in one year. We examined 936 STEMI patients who underwent either primary PCI or pharmacoinvasive reperfusion. A composite outcome was measured based on death, congestive heart failure, reinfarction or stroke prospectively ascertained during hospital stay and up to 1-year follow-up. The association between reperfusion strategy and the composite outcome was assessed using multivariate regression and Poisson proportional hazard model.Results:Compared to the pharmacoinvasive group, those undergoing primary PCI had higher Killip class on presentation and required more blood transfusions during hospitalization. There was no significant difference between primary PCI and pharmacoinvasive strategy with regards to the incidence of the composite outcome during the in-hospital period (RR = 1.0; 95% CI 0.98-1.02; p=0.96) after adjustment for possible confounders. Over one-year follow-up, the survival of the two groups was not different (p=0.66). The incidence of major bleeding was similar in both groups.Conclusions:STEMI patients treated with a pharmacoinvasive strategy have comparable outcomes to those treated with primary PCI with no increased risk of major bleeding. These real-world data support the use of a pharmacoinvasive strategy when primary PCI cannot be achieved in a timely fashion.