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Background Arterial stiffness can be separated into 2 main mechanisms: (1) load‐dependent stiffening from higher blood pressure and (2) structural stiffening due to remodeling of the vessel wall. The relationship between stiffness mechanisms and end organ damage is unknown. Methods and Results MESA (Multi‐Ethnic Study of Atherosclerosis) participants with carotid ultrasound were included in this study (n=6147). Carotid pulse wave velocity (cPWV) was calculated to represent total stiffness. Structural stiffness was calculated by adjusting cPWV to a 120/80 mm Hg blood pressure with participant‐specific models. Load‐dependent stiffness was the difference of total and structural stiffness. Associations with incident chronic kidney disease (CKD), dementia, and mortality were assessed with adjusted Cox models. During 14.3±4.8 years of follow‐up, 773 CKD events, 535 dementia events, and 1529 deaths occurred. Total cPWV was associated with mortality (hazard ratio [HR], per 1 m/s, 1.04 [95% CI, 1.01–1.08], P=0.02) and dementia (HR, 1.06 [95% CI, 1.01–1.12], P=0.03) but not CKD (HR, 1.03 [95% CI, 0.98–1.08], P=0.33). Structural cPWV was significantly associated with mortality (HR, 1.04 [95% CI, 1.00–1.08], P=0.04) but not CKD (HR, 1.00 [95% CI, 0.94–1.05], P=0.86) or dementia (HR, 1.06 [95% CI, 0.99–1.13], P=0.06). Load‐dependent cPWV was significantly associated with CKD (HR, 1.38 [95% CI, 1.17–1.63], P

Aim: Low-grade inflammation is known to facilitate the development of hypertensive organ damage. This study aimed to investigate the relationship between the leukocyte and lipid-based inflammation indices and asymptomatic organ damage (AOD) in treatment-naive and newly diagnosed hypertension patients (TNNDH). Methods: The study included 200 patients with TNNDH who are treating by the Cardiology Clinic and 100 healthy controls. Left venriculer mass index (LVMI) of >95 g/m2 in women and >115 g/m2 in men, and carotis intima media thickness (CIMT) of >0.9 mm or presence of plaque in the carotid artery and microalbuminuria of >30 mg/day were evaluated as AOD indicators. Platelet to lymphocyte ratio (PLR), neutrophil to lymphocyte ratio (NLR), systemic immune-inflammation index (SII), monocyte to HDL ratio (MHR), and atherogenic index of plasma (AIP) levels were calculated based on the complete blood count. Results: Positive correlations were found between all inflammation indices and AOD indicators. AOD was detected in 66.7% of the TNNDH patients. The mean PLR (143.0±37.9 vs. 138.0±36.2; p

Abstract Sustained by its relative ease of assessment, carotid artery intima-media thickness (cIMT) has emerged as an important surrogate marker of target organ damage in hypertensive heart disease over the last three decades. However, the prognostic utility of cIMT in hypertensive heart disease differs depending on its application. This review outlines cIMT and its prognostic utility among patients with hypertensive heart disease. It provides an overview of limitations of cIMT and areas for future research.

The present case is of 44-year-old woman who was a known case of sarcoidosis revealed granulomatous inflammation without caseafication. She also reported to suffer from proteinuria about 2 g/day, which was reported as Focal Segmental Glomerulosclerosis (FSGS) secondary to sarcoidosis after renal biopsy and thorough evaluation. Skeletal survey showed multiple lytic lesions in her skull, ribs, vertebra and iliac bone. The patient fully met diagnostic criteria for symptomatic Multiple Myeloma (MM) and chemotherapy was started with Velcade, Cyclophosphamide and Dexamethasone. Having completed chemotherapy, bone marrow plasma cells reached 8% and there were no peak of the serum or urine protein. Our patient is the first report of correlation of three diseases of Sarcoidosis and MM together and FSGS. Immune system impairment may be the main predisposing factor. The relationship between sarcoidosis and MM is unclear. Since in sarcoidosis, impaired immune system is involved, it predisposes developing malignancies in sarcoidosis. It is suggested that two important factors i.e. aneuploidy in the granuloma and peripheral blood lymphocytes can cause haematologic malignancy via developing genetic instability.

Abstract Hypertension is a major health concern in the developed world, and its prevalence increases with advancing age. The impact of hypertension on the function of the renal and cardiovascular systems is well studied; however, its influence on the brain regions important for cognition has garnered less attention. We utilized the Cyp1a1‐Ren2 xenobiotic‐inducible transgenic rat model to mimic both the age of onset and rate of induction of hypertension observed in humans. Male, 15‐month‐old transgenic rats were fed 0.15% indole‐3‐carbinol (I3C) chow to slowly induce renin‐dependent hypertension over a 6‐week period. Systolic blood pressure significantly increased, eventually reaching 200 mmHg by the end of the study period. In contrast, transgenic rats fed a control diet without I3C did not show significant changes in blood pressure (145 mmHg at the end of study). Hypertension was associated with cardiac, aortic, and renal hypertrophy as well as increased collagen deposition in the left ventricle and kidney of the I3C‐treated rats. Additionally, rats with hypertension showed reduced savings from prior spatial memory training when tested on the hippocampus‐dependent Morris swim task. Motor and sensory functions were found to be unaffected by induction of hypertension. Taken together, these data indicate a profound effect of hypertension not only on the cardiovascular‐renal axis but also on brain systems critically important for learning and memory. Future use of this model and approach may empower a more accurate investigation of the influence of aging on the systems responsible for cardiovascular, renal, and neurological health.

Variability in arterial pressure and cerebral blood flow has traditionally been interpreted as a marker of cardiovascular decompensation, and has been associated with negative clinical outcomes across varying time scales, from impending orthostatic syncope to an increased risk of stroke. Emerging evidence, however, suggests that increased hemodynamic variability may, in fact, be protective in the face of acute challenges to perfusion, including significant central hypovolemia and hypotension (including hemorrhage), and during cardiac bypass surgery. This review presents the dichotomous views on the role of hemodynamic variability on clinical outcome, including the physiological mechanisms underlying these patterns, and the potential impact of increased and decreased variability on cerebral perfusion and oxygenation. We suggest that reconciliation of these two apparently discrepant views may lie in the time scale of hemodynamic variability; short time scale variability appears to be cerebroprotective, while mid to longer term fluctuations are associated with primary and secondary end-organ dysfunction.