In response to the estimated potential impact of coronavirus disease (COVID-19) on New York City hospitals, our institution prepared for an influx of critically ill patients. Multiple areas of surge planning progressed, simultaneously focused on infection control, clinical operational challenges, ICU surge capacity, staffing, ethics, and maintenance of staff wellness. The protocols developed focused on clinical decisions regarding intubation, the use of high-flow oxygen, engagement with infectious disease consultants, and cardiac arrest. Mechanisms to increase bed capacity and increase efficiency in ICUs by outsourcing procedures were implemented. Novel uses of technology to minimize staff exposure to COVID-19 as well as to facilitate family engagement and end-of-life discussions were encouraged. Education and communication remained key in our attempts to standardize care, stay apprised on emerging data, and review seminal literature on respiratory failure. Challenges were encountered and overcome through interdisciplinary collaboration and iterative surge planning as ICU admissions rose. Support was provided for both clinical and nonclinical staff affected by the profound impact COVID-19 had on our city. We describe in granular detail the procedures and processes that were developed during a 1-month period while surge planning was ongoing and the need for ICU capacity rose exponentially. The approaches described here provide a potential roadmap for centers that must rapidly adapt to the tremendous challenge posed by this and potential future pandemics.

Several experimental and clinical evidences have linked an enhanced production of reactive oxygen species (ROS) to certain diseases of the cardiovascular system including hypertension and diabetes. However, it has never been clearly established whether the enhanced oxidative stress observed in those conditions is primary or secondary to the pathological process. Our experimental studies have permitted to demonstrate that ROS, mainly through the production of superoxide anion, can cause important alterations in the cellular signal transduction systems characterized by an enhanced production of inositol triphosphate and a reduced production of cyclic GMP in cultured vascular smooth muscle cells (SMC), thus favouring the vasoconstriction. Since those effects were found to be increased in SMC from spontaneously hypertensive rats (SHR), this suggested a greater sensitivity of the vascular tissue of SHR to the oxidative stress. Moreover, we also have observed an increased production of superoxide anion in the aorta of rats made hypertensive according to the SHR, glucose or angiotensin-induced and DOCA-salt models during the development of hypertension. Since the superoxide anion production could be correlated with the level of blood pressure and since the development of hypertension could be either totally prevented or markedly attenuated by chronic treatment with potent antioxidative therapies such as alpha lipoic acid or aspirin, this suggested a major contribution of vascular superoxide anion production in the development of hypertension in those models. Moreover, the development of insulin resistance, which is associated to the model of glucose-induced hypertension, was also found to be prevented by chronic antioxidant therapies, thus suggesting that oxidative stress plays an important role as well in the development of insulin resistance and type 2 diabetes. In conclusion, it appears that oxidative stress may constitute a major pathogenic factor in the development of hypertension and type 2 diabetes. Moreover, our studies suggest that the chronic treatment with appropriate antioxidative therapies could prevent the development of hypertension and diabetes as well as their complications in various experimental models of hypertension.

Independent from sex, increased height is significantly associated with the risk of AF.

This study represents the largest cohort of patients hospitalized with HFpEF to date, yielding the following observations: number of hospitalizations for HFpEF was comparable with that of HFrEF; patients with HFpEF were most often women and elderly, with a high burden of comorbidities; outcomes appeared improved among a subset of patients; pulmonary hypertension, liver disease, and chronic renal failure were strongly associated with poor outcomes.

The transient increase in norepinephrine levels observed with NPA and the sustained increases in norepinephrine levels observed after chronic treatment with amlodipine suggest that sympathetic activation occurs with those two drugs. The lack of increase in norepinephrine levels after administration of NGITS suggests that this formulation does not activate the sympathetic system. The lowering of epinephrine levels after administrations of NGITS and amlodipine suggests that inhibition of release of epinephrine by the adrenal medulla occurs with longer-acting dihydropyridine formulations.