Environmental Pollution and Cardiovascular Disease: Part 2 of 2: Soil, Water, and Other Forms of Pollution.

With a growing body of evidence that now links environmental pollution to adverse cardiovascular disease (CVD) outcomes, pollution has emerged as an important risk factor for CVD. There is thus an urgent need to better understand the role of pollution in CVD, key pathophysiological mechanisms, and to raise awareness among health care providers, the scientific community, the general population, and regulatory authorities about the CV impact of pollution and strategies to reduce it. This article is part 2 of a 2-part state-of-the-art review on the topic of pollution and CVD-herein we discuss major environmental pollutants and their effects on CVD, highlighting pathophysiological mechanisms, and strategies to reduce CVD risk.

Environmental Pollution and Cardiovascular Disease: Part 1 of 2: Air Pollution.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Over the past 50 years, there has been a substantial decline in the incidence of CVD and related mortality in high-income countries, largely due to the mitigation of modifiable risk factors such as smoking, hypertension, and diabetes. However, a significant burden of CVD remains in low- to middle-income countries, despite their lower prevalence of traditional risk factors; other environmental factors, particularly pollution, play a significant role in this attributable risk. Mounting evidence underscores a strong association between pollution and adverse health effects, including CVD. This article is part 1 of a 2-part state-of-the-art review and discusses air pollution and its adverse effects on CVD, highlighting pathophysiological mechanisms and methods to reduce air pollution and exposure to these pollutants.

Myocarditis in the Setting of Recent COVID-19 Vaccination.

We report three patients who presented with chest pain after receiving either the BNT162b2 Pfizer/BioNTech or mRNA-1273 Moderna/NIH vaccine. Clinical presentation, biomarker, and cardiac MRI supported myocarditis. It is imperative that potential side effects of COVID-19 vaccine are reported to improve our knowledge about COVID-19 and mRNA vaccines.

Association of hypokalemia with an increased risk for medically treated arrhythmias.

BACKGROUND: Potassium replenishment protocols are often employed across broad patient populations to prevent cardiac arrhythmias. Tailoring potassium thresholds to specific patient populations would reduce unnecessary tasks and cost. The objective of this retrospective cohort study was to determine the threshold at which hypokalemia increases the risk for medically treated arrhythmias in cardiac versus medical and surgical intensive care units. METHODS: Patients captured in the publicly available Philips eICU database were assessed for initiation of either intravenous amiodarone, adenosine, ibutilide, isoproterenol, or lidocaine as a surrogate for a clinically significant arrhythmia. A landmark time-to-event analysis was conducted to investigate the association of serum potassium values and time-marked administration of an antiarrhythmic drug. Analysis was adjusted for comorbidities, the use of vasopressor agents, diuretics, as well as age, gender and severity of illness. RESULTS: Among 20,665 admissions to cardiac intensive care units, 1,371 (6.6%) were treated with either amiodarone, adenosine, ibutilide, isoproterenol, or lidocaine. For potassium values of ≥3.0<3.5mEq/L, antiarrhythmic treatment occurred at an increased rate compared to a baseline of ≥4.0≤5.0mEq/L (HR 1.23, 95% CI 1.01-1.51; P = 0.04). For admissions to medical and surgical intensive care units, 2,100 of 69,714 patients (3.0%) were treated with either amiodarone, adenosine, ibutilide, isoproterenol, or lidocaine. Potassium values of ≥3.0<3.5mEq/L were also associated with an increased hazard of treatment (HR 1.26, 95% CI 1.09-1.45; P = 0.002). In both cohorts, worsening hypokalemia was associated with an increased risk of antiarrhythmic drug treatment. In neither cohort were there statistically significant differences for serum potassium values of ≥3.5<4.0 and a baseline of ≥4.0≤5.0mEq/L. The proportion of patients initiated on vasopressors or inotropes was over four-fold higher in those treated with one of the antiarrhythmic drugs in both cohorts. CONCLUSIONS: Serum potassium levels <3.5mEq/L were associated with an increased hazard for treatment with specific antiarrhythmic drugs in a large cohort of patients admitted to both a cardiac as well as medical and surgical intensive care units. Potassium thresholds may be individualized further based on risk of relevant outcomes.

Chest Pain During Chemotherapy: A Case of Severe Myocardial Bridging.

A cancer patient presented with acute chest pain at rest 40 hours after IV fluorouracil infusion. Angiography showed evidence of myocardial bridging.

Novel Method for Exchange of Impella Circulatory Assist Catheter: The "Trojan Horse" Technique.

Patients with an indwelling Impella may require escalation of hemodynamic support or exchange to another circulatory assistance platform. As such, preservation of vascular access is preferable in cases where anticoagulation cannot be discontinued or to facilitate exchange to an alternative catheter or closure device. Challenges exist in avoiding bleeding and loss of wire access in these situations. We describe a single-access "Trojan Horse" technique that minimizes bleeding while maintaining arterial access for rapid exchange of this percutaneous ventricular assist device.

Advantages and pitfalls of pocket ultrasound vs daily chest radiography in the coronary care unit: A single-user experience.

BACKGROUND: Pocket ultrasonography may enhance patient diagnosis and care. We sought to assess pocket ultrasound in detecting common conditions in the coronary care unit (CCU) compared to portable daily chest radiography (CXR) and conventional transthoracic echocardiography (TTE). METHODS: An experienced pocket ultrasound user performed a pocket ultrasound examination for interstitial edema, pneumonia, central line seen in the right ventricle, pleural and pericardial effusions, left atrial enlargement, and cardiomegaly. Data were blindly compared to the radiologist CXR interpretation and cardiologist TTE interpretation. RESULTS: A total of 102 CXR and pocket ultrasound examinations were performed in 66 patients. The most common CXR indication was "interval change" (37%) and finding central line (65%). Pocket ultrasound demonstrated overall good concordance with CXR ranging from 77% for pleural effusion to 92% for pneumonia. Additionally, the pocket ultrasound examination appeared to anticipate resolution of pulmonary edema prior to the CXR. Compared to TTE, pocket ultrasound had excellent sensitivity for cardiac findings with values ranging from 85% for left atrial enlargement to 100% for cardiomegaly, but limited specificity of cardiomegaly at just 51%. CONCLUSION: In the CCU, bedside pocket ultrasound reliably diagnoses common conditions identified by CXR with the advantage of lack of ionizing radiation and the suggestion of detecting the resolution of pulmonary edema prior to CXR. Pitfalls include only modest concordance for pleural effusions and limited specificity for cardiomegaly. Larger, multicenter studies are needed to determine whether pocket ultrasound can reduce routine daily CXR in the CCU and other intensive care settings.

Bridging the Health Data Divide.

Fundamental quality, safety, and cost problems have not been resolved by the increasing digitization of health care. This digitization has progressed alongside the presence of a persistent divide between clinicians, the domain experts, and the technical experts, such as data scientists. The disconnect between clinicians and data scientists translates into a waste of research and health care resources, slow uptake of innovations, and poorer outcomes than are desirable and achievable. The divide can be narrowed by creating a culture of collaboration between these two disciplines, exemplified by events such as datathons. However, in order to more fully and meaningfully bridge the divide, the infrastructure of medical education, publication, and funding processes must evolve to support and enhance a learning health care system.

A case of hypercalcemia secondary to hot tub lung.

Hypersensitivity pneumonitis (HP) is a diffuse granulomatous lung disease resulting from inhalation of an antigen to which an individual has been previously sensitized. Hot tub lung is an increasingly common form of HP associated with inhalation of water aerosols containing Mycobacterium avium complex organisms that contaminate hot tub water. Granulomatous lung disorders, most classically sarcoidosis, have been associated with unregulated 1-α-hydroxylase expression by macrophages present in the granulomas, causing conversion of 25-OH-vitamin D to the active form of vitamin D, 1,25(OH)2 vitamin D, and, thus, hypercalcemia. To our knowledge, this is the first confirmed case of hypercalcemia secondary to elevated 1,25(OH)2 vitamin D levels associated with HP.

Feasibility of remote real-time guidance of a cardiac examination performed by novices using a pocket-sized ultrasound device.

Background. The potential of pocket-sized ultrasound devices (PUDs) to improve global healthcare delivery is limited by the lack of a suitable imaging protocol and trained users. Therefore, we investigated the feasibility of performing a brief, evidence-based cardiac limited ultrasound exam (CLUE) through wireless guidance of novice users. Methods. Three trainees applied PUDs on 27 subjects while directed by an off-site cardiologist to obtain a CLUE to screen for LV systolic dysfunction (LVSD), LA enlargement (LAE), ultrasound lung comets (ULC+), and elevated CVP (eCVP). Real-time remote audiovisual guidance and interpretation by the cardiologist were performed using the iPhone 4/iPod (FaceTime, Apple, Inc.) attached to the PUD and transmitted data wirelessly. Accuracy and technical quality of transmitted images were compared to on-site, gold-standard echo thresholds. Results. Novice versus sonographer imaging yielded technically adequate views in 122/135 (90%) versus 130/135 (96%) (P < 0.05). CLUE's combined SN, SP, and ACC were 0.67, 0.96, and 0.90. Technical adequacy (%) and accuracy for each abnormality (n) were LVSD (85%, 0.93, n = 5), LAE (89%, 0.74, n = 16), ULC+ (100%, 0.94, n = 5), and eCVP (78%, 0.91, n = 1). Conclusion. A novice can perform the CLUE using PUD when wirelessly guided by an expert. This method could facilitate PUD use for off-site bedside medical decision making and triaging of patients.

A PPARγ-FGF1 axis is required for adaptive adipose remodelling and metabolic homeostasis.

Although feast and famine cycles illustrate that remodelling of adipose tissue in response to fluctuations in nutrient availability is essential for maintaining metabolic homeostasis, the underlying mechanisms remain poorly understood. Here we identify fibroblast growth factor 1 (FGF1) as a critical transducer in this process in mice, and link its regulation to the nuclear receptor PPARγ (peroxisome proliferator activated receptor γ), which is the adipocyte master regulator and the target of the thiazolidinedione class of insulin sensitizing drugs. FGF1 is the prototype of the 22-member FGF family of proteins and has been implicated in a range of physiological processes, including development, wound healing and cardiovascular changes. Surprisingly, FGF1 knockout mice display no significant phenotype under standard laboratory conditions. We show that FGF1 is highly induced in adipose tissue in response to a high-fat diet and that mice lacking FGF1 develop an aggressive diabetic phenotype coupled to aberrant adipose expansion when challenged with a high-fat diet. Further analysis of adipose depots in FGF1-deficient mice revealed multiple histopathologies in the vasculature network, an accentuated inflammatory response, aberrant adipocyte size distribution and ectopic expression of pancreatic lipases. On withdrawal of the high-fat diet, this inflamed adipose tissue fails to properly resolve, resulting in extensive fat necrosis. In terms of mechanisms, we show that adipose induction of FGF1 in the fed state is regulated by PPARγ acting through an evolutionarily conserved promoter proximal PPAR response element within the FGF1 gene. The discovery of a phenotype for the FGF1 knockout mouse establishes the PPARγ­FGF1 axis as critical for maintaining metabolic homeostasis and insulin sensitization.

Role of agouti-related protein-expressing neurons in lactation.

Hypothalamic neurons that express agouti-related protein (AgRP) and neuropeptide Y (NPY) are thought to be important for regulation of feeding, especially under conditions of negative energy balance. The expression of NPY and AgRP increases during lactation and may promote the hyperphagia that ensues. We explored the role of AgRP neurons in reproduction and lactation, using a mouse model in which AgRP-expressing neurons were selectively ablated by the action of diphtheria toxin. We show that ablation of AgRP neurons in neonatal mice does not interfere with pregnancy, parturition, or lactation, suggesting that early ablation allows compensatory mechanisms to become established. However, ablation of AgRP neurons after lactation commences results in rapid starvation, indicating that both basal feeding and lactation-induced hyperphagia become dependent on AgRP neurons in adulthood. We also show that constitutive inactivation of Npy and Agrp genes does not prevent pregnancy or lactation, nor does it protect lactating dams from diphtheria toxin-induced starvation.

NPY/AgRP neurons are not essential for feeding responses to glucoprivation.

Animals respond to hypoglycemia by eating and by stimulating gluconeogenesis. These responses to glucose deprivation are initiated by glucose-sensing neurons in the brain, but the neural circuits that control feeding behavior are not well established. Neurons in the arcuate region of the hypothalamus that express neuropeptide Y (NPY) and agouti-related protein (AgRP) have been implicated in mediating the feeding response to glucoprivation. We devised a method to selectively ablate these neurons in neonatal mice and then tested adult mice for their feeding responses to fasting, mild hypoglycemia, 2-deoxy-d-glucose and a ghrelin receptor agonist. Whereas the feeding response to the ghrelin receptor agonist was completely abrogated, the feeding response to glucoprivation was normal. The feeding response after a fast was attenuated when standard chow was available but normal with more palatable solid or liquid diet. We conclude that NPY/AgRP neurons are not necessary for generating or mediating the orexigenic response to glucose deficiency, but they are essential for the feeding response to ghrelin and refeeding on standard chow after a fast.