Circulating fibrocyte levels correlate with left ventricular mass in middle-aged healthy adults without hypertension.

Background: Fibrocytes, circulating bone-marrow derived cells that differentiate into fibroblasts and myofibroblasts, are a major source of hypertensive arterial fibrosis and correlate with left ventricular (LV) mass in subjects with hypertension. We tested whether circulating fibrocytes levels correlate with LV mass in middle-aged adults without hypertension. Methods: We measured peripheral blood fibrocyte levels and their activated phenotypes in 13 middle-aged, non-hypertensive adults and performed cardiac magnetic resonance imaging to assess LV mass. Results: There was a strong correlation between total fibrocyte levels (CD45 + Col1+) and LV mass index (r = 0.71, p = 0.006), as well as fibrocyte subsets expressing the chemokine markers CCR2 (r = 0.60, p = 0.032), CCR5 (r = 0.62, p = 0.029), CCR7 (r = 0.60, p = 0.034), co-expression of CXCR4 and CCR2 (r = 0.62, p = 0.029), α-SMA+ (r = 0.57, p = 0.044), CD133 (r = 0.59, p = 0.036), and pSTAT6 (r = 0.64, p = 0.032). Conclusions: Circulating fibrocytes are associated with LV mass index in middle-aged, non-hypertensive adults and may be a harbinger for the development of hypertension.

Anisocoria in patients with hyperhidrosis: A case series for the primary care physician.

The differential diagnosis for anisocoria is broad and ranges from benign to life-threatening causes. Often, patients with new onset anisocoria present to their primary care physician, an urgent care center, or an emergency room. As such, it is important for non-ophthalmologist physicians to be familiar with its common causes. We present two cases of pharmacologic anisocoria from Qbrexza (glycopyronnium), a wipe used in the treatment of hyperhidrosis. Identifying this medication as a cause of anisocoria in patients with hyperhidrosis can reduce costs and unnecessary testing. Furthermore, physician education about safer usage can be provided.

Microvascular Dysfunction as a Systemic Disease: A Review of the Evidence.

Microvascular dysfunction describes a varied set of conditions that includes vessel destruction, abnormal vasoreactivity, in situ thrombosis, and fibrosis, which ultimately results in tissue damage and progressive organ failure. Microvascular dysfunction has a wide array of clinical presentations, ranging from ischemic heart disease to renal failure, stroke, blindness, pulmonary arterial hypertension, and dementia. An intriguing unifying hypothesis suggests that microvascular dysfunction of specific organs is an expression of a systemic illness that worsens with age and is accelerated by vascular risk factors. Studying relationships across a spectrum of microvascular diseases affecting the brain, retina, kidney, lung, and heart may uncover shared pathologic mechanisms that could inform novel treatment strategies. We review the evidence that supports the notion that microvascular dysfunction represents a global pathologic process. Our focus is on studies reporting concomitant microvascular dysfunction of the heart with that of the brain, kidney, retina, and lung.

Critical role of the coronary microvasculature in heart disease: From pathologic driving force to "innocent" bystander.

The coronary microvasculature is responsible for providing oxygen and nutrients to myocardial tissue. A healthy microvasculature with an intact and properly functioning endothelium accomplishes this by seemless changes in vascular tone to match supply and demand. Perturbations in the normal physiology of the microvasculature, including endothelial and/or vascular smooth muscle dysfunction, result in impaired function (vasoconstriction, antithrombotic, etc.) and structural (hypertrophic, fibrotic) abnormalities that lead to microvascular ischemia and potential organ damage. While coronary microvascular dysfunction (CMD) is the primary pathologic driving force in ischemia with non-obstructive coronary artery disease (INOCA), angina with no obstructive coronary arteries (ANOCA), and myocardial infarction with non-obstructed coronary arteries (MINOCA), it may be a bystander in many cardiac disorders which later become pathologically associated with signs and/or symptoms of myocardial ischemia. Importantly, regardless of the primary or secondary basis of CMD in the heart, it is associated with important increases in morbidity and mortality. In this review we discuss salient features pertaining to known pathophysiologic mechanisms driving CMD, the spectrum of heart diseases where it places a critical role, invasive and non-invasive diagnostic testing, management strategies, and the gaps in knowledge where future research efforts are needed.