Computed tomography evaluation of patent paraumbilical vein and its aneurysm in relation to other portosystemic collateral channels in patients with liver cirrhosis and portal hypertension

Purpose: The aim of the study was to evaluate the relationship between the diameter and aneurysmal dilatation of the paraumbilical vein (PUV) and the presence of portosystemic collateral shunts and their relationship with age and portal vein diameter. Material and methods: The retrospective analysis, performed in the II Department of Radiology, Medical University Hospital in Warsaw, included 126 patients (77 males and 49 females) with patent umbilical vein and signs of portal hypertension due to liver cirrhosis. All patients underwent contrast enhanced abdominal CT. The average age was 54.7 ±12.98. We analysed the number and type of portosystemic collateral channels in respect of age, sex, presence of oesophageal varices, and the diameter of the paraumbilical vein and the portal vein. Results: Our results disclosed statistically significant negative correlation between patient age and diameter of paraumbilical vein, number of portosystemic collateral channels and diameter of portal vein and positive correlation between diameter of paraumbilical vein and diameter of portal vein. A statistically significant difference in diameter of portal vein and number of collateral channels was found in groups with and without oesophageal varices. No significant difference in age and portal vein diameter was found in these groups. Conclusions: Our study showed that younger patients with liver cirrhosis are characterised by wider paraumbilical veins and higher number of portosystemic collateral channels. The presence of oesophageal varices does not correlate with age, sex, diameter of paraumbilical vein, and number of collateral portosystemic channels

Computed tomography evaluation of patent paraumbilical vein and its aneurysm in relation to other portosystemic collateral channels in patients with liver cirrhosis and portal hypertension

Purpose: The aim of the study was to evaluate the relationship between the diameter and aneurysmal dilatation of the paraumbilical vein (PUV) and the presence of portosystemic collateral shunts and their relationship with age and portal vein diameter. Material and methods: The retrospective analysis, performed in the II Department of Radiology, Medical University Hospital in Warsaw, included 126 patients (77 males and 49 females) with patent umbilical vein and signs of portal hypertension due to liver cirrhosis. All patients underwent contrast enhanced abdominal CT. The average age was 54.7 ±12.98. We analysed the number and type of portosystemic collateral channels in respect of age, sex, presence of oesophageal varices, and the diameter of the paraumbilical vein and the portal vein. Results: Our results disclosed statistically significant negative correlation between patient age and diameter of paraumbilical vein, number of portosystemic collateral channels and diameter of portal vein and positive correlation between diameter of paraumbilical vein and diameter of portal vein. A statistically significant difference in diameter of portal vein and number of collateral channels was found in groups with and without oesophageal varices. No significant difference in age and portal vein diameter was found in these groups. Conclusions: Our study showed that younger patients with liver cirrhosis are characterised by wider paraumbilical veins and higher number of portosystemic collateral channels. The presence of oesophageal varices does not correlate with age, sex, diameter of paraumbilical vein, and number of collateral portosystemic channels

Canagliflozin and renal outcomes in type 2 diabetes and nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to <90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

Malignant Hypertension:A Systemic Cardiovascular Disease: JACC Review Topic of the Week.

Malignant hypertension (MHT) is a hypertensive emergency with excessive blood pressure (BP) elevation and accelerated disease progression. MHT is characterized by acute microvascular damage and autoregulation failure affecting the retina, brain, heart, kidney, and vascular tree. BP must be lowered within hours to mitigate patient risk. Both absolute BP levels and the pace of BP rise determine risk of target-organ damage. Nonadherence to the antihypertensive regimen remains the most common cause for MHT, although antiangiogenic and immunosuppressant therapy can also trigger hypertensive emergencies. Depending on the clinical presentation, parenteral or oral therapy can be used to initiate BP lowering. Evidence-based outcome data are spotty or lacking in MHT. With effective treatment, the prognosis for MHT has improved; however, patients remain at high risk of adverse cardiovascular and kidney outcomes. In this review, we summarize current viewpoints on the epidemiology, pathogenesis, and management of MHT; highlight research gaps; and propose strategies to improve outcomes

Altered monocytic phenotypes are linked to hypertension form - a clinical observational study

No abstract available

Cardiac Phenotypes in Secondary Hypertension: JACC State-of-the-Art Review.

Several forms of secondary hypertension carry a high risk of cardiac morbidity and mortality. Evaluation of cardiac phenotypes in secondary hypertension provides a unique opportunity to study underlying hormonal and biochemical mechanisms affecting the heart. We review the characteristics of cardiac dysfunction in different forms of secondary hypertension and clarify the mechanisms behind the higher prevalence of heart damage in these patients than in those with primary hypertension. Attention to the specific clinical/biochemical phenotypes of these conditions may assist clinicians to screen for and confirm secondary forms of hypertension. Thereby, early signs of heart damage can be recognized and monitored, allowing individualized treatment to delay or prevent evolution toward more advanced disease

Current progress in clinical, molecular, and genetic aspects of adult fibromuscular dysplasia.

Fibromuscular dysplasia (FMD) is a non-atherosclerotic vascular disease that may involve medium-sized muscular arteries throughout the body. The majority of FMD patients are women. Although a variety of genetic, mechanical, and hormonal factors play a role in the pathogenesis of FMD, overall, its cause remains poorly understood. It is probable that the pathogenesis of FMD is linked to a combination of genetic and environmental factors. Extensive studies have correlated the arterial lesions of FMD to histopathological findings of arterial fibrosis, cellular hyperplasia, and distortion of the abnormal architecture of the arterial wall. More recently, the vascular phenotype of lesions associated with FMD has been expanded to include arterial aneurysms, dissections, and tortuosity. However, in the absence of a string-of-beads or focal stenosis, these lesions do not suffice to establish the diagnosis. While FMD most commonly involves renal and cerebrovascular arteries, involvement of most arteries throughout the body has been reported. Increasing evidence highlights that FMD is a systemic arterial disease and that subclinical alterations can be found in non-affected arterial segments. Recent significant progress in FMD-related research has led to improve our understanding of the disease's clinical manifestations, natural history, epidemiology, and genetics. Ongoing work continues to focus on FMD genetics and proteomics, physiological effects of FMD on cardiovascular structure and function, and novel imaging modalities and blood-based biomarkers that can be used to identify subclinical FMD. It is also hoped that the next decade will bring the development of multi-centred and potentially international clinical trials to provide comparative effectiveness data to inform the optimal management of patients with FMD