Physiological organ cross-talk is necessary to maintain equilibrium and homeostasis. Heart and kidney are the essences of this equilibrium. Organ failure in either of these organs can perturb the bidirectional communication between them, impinging this unpleasant vascular and cellular milieu on other distant organs. Cardiorenal syndrome (CRS) type I occurs due to acute deterioration of cardiac function, ultimately causing acute kidney injury (AKI). This syndrome is an intricate condition with neurohormonal and inflammatory aspects. Inflammation creates a vicious circle filled with the innate and adaptive immune systems, pro-inflammatory cytokines, chemokines to actuate hemodynamic compromise in CRS type I patients. Proinflammatory cytokines not only aggravate fluid retention and venous congestion but also initiate apoptosis and oxidative stress. The immune response's primary motive is to elicit the heart and kidney to produce cytokines, intensifying the inflammatory process. Despite the possible standard of care, patient mortality, treatment cost, readmissions are extreme in CRS type I, and inflammation certainly has critical inferences warranting future research in humans.
Gastrointestinal bleeding due to angiodysplasia is a common problem in patients with renal insufficiency. There are several theories to explain the increased occurrence of these lesions in this specific group of patients, including various metabolic factors and existence of comorbidities. Advancements made in diagnostic measures have helped route the approach in patients with different risk factors and have also helped solve the dual purpose involving therapeutic intervention with endoscopy. We conducted a thorough literature search on PubMed to extract relevant data. A total of 29 articles were chosen after applying the inclusion and exclusion criteria. Although the clinical presentations may vary in this cohort of patients, and bleeding is known to stop spontaneously, a conservative approach may not be enough. Endoscopic treatment, use of hormones like estrogen, octreotide, and vasopressin, arterial embolization, and lastly surgery are valuable therapeutic tools.
Objectives: This study aimed to compare short- and long-term outcomes following various alternative access routes for transcatheter aortic valve replacement (TAVR).
Background: Several studies have pair-wise compared access sites for TAVR but pooled estimate of overall comparative efficacy and safety outcomes are not well known.
Methods: Thirty-four studies with a pooled sample size of 30,986 records were selected by searching PubMed and Cochrane library databases from inception through 11th June 2021 for patients undergoing TAVR via 1 of 6 different access sites: Transfemoral (TF), Transaortic (TAO), Transapical (TA), Transcarotid (TC), Transaxillary/Subclavian (TSA), and Transcaval (TCV). Data extracted from these studies were used to conduct a frequentist network meta-analysis with a random-effects model using TF access as a reference group.
Results: Compared with TF, both TAO [RR 1.91, 95% CI (1.46-2.50)] and TA access [RR 2.12, 95%CI (1.84-2.46)] were associated with an increased risk of 30-day mortality. No significant difference was observed for stroke, myocardial infarction, major bleeding, conversion to open surgery, and major adverse cardiovascular or cerebrovascular events in the short-term (≤30 days). Major vascular complications were lower in TA [RR 0.43, (95% CI, 0.28-0.67)] and TC [RR 0.51, 95% CI (0.35-0.73)] access compared to TF. The 1-year mortality was higher in the TAO [RR of 1.35, (95% CI, 1.01-1.81)] and TA [RR 1.44, (95% CI, 1.14-1.81)] groups.
Conclusion: Non-thoracic alternative access site utilization for TAVR implantation (TC, TSA and TCV) is associated with similar outcomes to conventional TF access. Thoracic TAVR access (TAO and TA) is associated with increased short and long-term mortality.
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