Intravascular administration of iodinated contrast media is an essential tool for the imaging of blood vessels and cardiac chambers, as well as for percutaneous coronary and structural interventions. Along with the spreading of diagnostic and interventional procedures, the increasing incidence of contrast-induced nephropathy (CIN) has become an important and prognostically relevant problem. CIN is thought to be largely dependent on oxidative damage, and is a considerable cause of renal failure, being associated with prolonged hospitalization and significant morbidity/mortality. The most effective treatment strategy of this serious complication remains prevention, and several preventive measures have been extensively investigated in the last few years. Preprocedural hydration is the best-known and mostly accepted strategy. The administration of sodium bicarbonate has controversial effects, and is likely to be ineffective when the infused dose is unable to achieve adequate urine alkalinization. Since alkaline pH suppresses the production of free radicals, increasing urine pH would be an attractive goal for CIN prevention. In a prospective randomized controlled, open-label clinical trial we will test the hypothesis that urine alkalinization with either oral or intravenous bicarbonate on top of hydration alone is the main determinant of CIN prevention (primary endpoint) in a population of patients with moderate or severe chronic kidney disease scheduled for coronary angiography and/or angioplasty. If we then demonstrate nonsignificant differences in urine alkalinization and incidence of CIN between the two bicarbonate groups (secondary endpoint), a practical implication will be that oral administration is preferable for practical reasons over the administration of intravenous bicarbonate.
BackgroundAbnormalities of the mitral valve (MV) apparatus are typical features of hypertrophic cardiomyopathy (HCM). These abnormalities include leaflet elongation, thick leaflets, displacement of papillary muscle, and systolic anterior motion (SAM) of the MV anterior leaflet. Mitral valve chordal rupture associated with HCM is a rare but serious issue capable of change the clinical apparence and the prognosis of the patient.Case summaryA 57-year-old lady with a history of diabetes, dyslipidemia, and a previous single episode of atrial fibrillation (treated with pharmacological cardioversion), presented to the Emergency Department for worsening dyspnea (New York Heart Association Classification class IV). A trans-thoracic echocardiogram (TTE) showed a significant, septal, and asymmetric left ventricular hypertrophy (basal anteroseptal wall diastolic thickness of 19 mm) with normal left ventricle systolic function. A SAM of AML was evident together with a left ventricular outflow tract gradient of 56 mmHg at rest, rising to 136 mmHg during the Valsalva maneuver. In addition, there was evidence of moderate to severe mitral regurgitation (MR) with an anteriorly directed jet, not very typical of MR related to SAM. A 2D-3D trans-esophageal echocardiogram (2D-3D TEE) revealed a combined MR mechanism based on PML degenerative prolapse with P2-flail from ruptured chordae with related eccentric anteriorly directed regurgitant jet, together with a second regurgitant posteriorly directed jet, related to SAM of AML. The patient underwent MV repair together with septal myectomy, with a good final outcome.ConclusionPre-operative echocardiography (both TTE and 2D-3D TEE) is an essential tool in order to detect different MV abnormalities in patients with HCM. These types of patients should never be treated by septal reduction alone. Surgical MV repair or replacement, together with septal myectomy, may be the preferred approach.
This case describes a peculiar aetiology of severe aortic regurgitation and LVOT obstruction in a young adult with bilateral congenital cataract and uncontrolled hypertension, who presented with heart failure and was found to suffer from aortic valve degeneration with fibromuscular metaplasia and cusp delamination.
Aims Contrast-induced acute kidney injury (CI-AKI) after coronary angiography and percutaneous interventions (PCI) impacts on hospitalization duration and mortality. Pre-procedural hydration is the sole strategy currently recommended for preventing CI-AKI. The role of sodium bicarbonate (SB) although attractive, since urine alkalinization suppresses the production of reactive oxygen species, is still controversial, and the optimal dosing to attain adequate urine alkalinization is still undefined. The PrevenTion of contrast-inducEd nephropathy with urine alkalinization (TEATE) study was a prospective 3-centre 3-arm single-blind randomized controlled trial testing the hypothesis that adequate urine alkalinization is associated with CI-AKI prevention. Secondary endpoints were the efficacy of SB vs. saline in achieving adequate urine alkalinization and reducing the incidence of CI-AKI compared with saline. Methods and results Patients candidate to coronary angiography and/or PCI with moderate-to-severe chronic kidney disease [eGFR of 15–60 ml/min/1.73 m2, by the Modification of Diet in Renal Disease Study equation (MDRD)] were randomly assigned to saline hydration (control), oral SB or i.v. SB. The study protocol was registered (ClinicalTrials.gov NCT02980003). We evaluated urinary pH at the time of hospitalization, immediately before coronary angiography and 24–48 h after angiography. According to urine pH immediately before the procedure, patients were divided in two groups above or below a pH cut-off of 6. We enrolled a total of 241 patients: 81 were randomly assigned to the control group, 82 to i.v. SB and 78 to oral SB. Patients achieving a urinary pH > 6 before angiography had a lower incidence of CI-AKI (46%) than patients with urinary pH ≤ 6 (54%) [OR = 0.48 (95% CI: 0.25–0.9), P = 0.023]. The number of patients with urine pH > 6 was higher in both the i.v. (71%) and the oral SB (65%) groups compared to the hydration-only group (44%, P = 0.004). We found however no difference in the incidence of CI-AKI in the three treatment arms (20% in hydration alone, 21% in oral SB group and 22% in i.v. SB group) (P = 0.94). Subgroup analyses according to basal urine pH and eGFR ranges failed to identify statistically significant differences in the development of CI-AKI according to treatment allocation. Conclusions Urinary pH before the administration of contrast medium is an inverse correlate of CI-AKI incidence, and SB is superior to hydration alone in achieving urinary alkalinization. Since, however, SB did not reduce the incidence of CI-AKI, we conclude that urinary pH is a marker and not a mediator of CI-AKI.
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