Research has demonstrated the disproportionate quality of care for women with cardiovascular disease. These findings have prompted a renewed focus on cardiovascular disease awareness and disease prevention in women. Spontaneous coronary artery dissection (SCAD) is a significant cause of myocardial infarction (MI) and sudden death that primarily affects women. ongoing research has led to improved diagnostic capabilities and changes in approaches to initial and long-term management most importantly this research has provided evidence that SCAD is more common than previously thought and must be evaluated and treated differently from atherosclerotic MI. The difference between SCAD and atherosclerotic MI is highlighted in high rates of recurrent disease, gender distribution, association with exogenous hormones, pregnancy, migraine, physical and emotional stress triggers, concurrent systemic arteriopathies, and connective tissue disease. In this review, we provide updated insights and a summary of the epidemiology, risk factors, clinical presentation, diagnosis, treatment options, prognosis, and recurrence prevention of SCAD. We aim to provide a review of SCAD as a focus on cardiovascular disease awareness and disease prevention in women.

We developed an optimized Dipheylthiocarbazone or Dithizone (DTZ) with improved physical and chemical properties to characterize human islets and insulin-producing cells differentiated from embryonic stem cells. Application of the newly formulated iDTZ (i stands for islet) over a range of temperatures, time intervals and cell and tissue types found it to be robust for identifying these cells. Through high transition zinc binding, the iDTZ compound concentrated in insulin-producing cells and proved effective at delineating zinc levels in vitro .

In the setting of the raging COVID-19 pandemic, the search for innovative therapeutics is desperately sought after. As we learn more about the characteristics and metabolic health of patients and as our understanding of COVID-19 pathophysiology and treatment progresses, so is our understanding of medication effects that might increase disease severity. As of late, ACE inhibitors have been under investigation for a potential increase in illness severity due to ACE2 upregulation. Given our knowledge of other nutrient-pharmaceutical interactions, could the ACE inhibitor impact on COVID be due to something else? In this paper, we discuss the possibility that ACE inhibitors might be affecting COVID-19 patients by causing zinc insufficiency. KEY MESSAGES Zinc deficiency caused by chronic ACE inhibitor usage may exacerbate the pathogenicity of COVID-19 in susceptible patients. A multi-center study is needed to assess the zinc levels of patients with COVID-19 who are taking ACE inhibitors and other medications that may result in low zinc levels.

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