M a i l i n g A d d r e s s : F r e d e r i c o T. U l t r a m a r i @@@@@@@@@@@@@@@@@@@@@@@@@@@ It is estimated that 6,000 and 2,000 cardiac catheterization procedures per million inhabitants/year are performed in Western countries for diagnostic and therapeutic purposes. In order to perform these procedures, 1,800 tons of iodine are required all over the world to manufacture contrast media (CM). The number of procedures that require the use of contrast media (or dye) has increased over time, and the population submitted to it is growing older, presenting more comorbidities 1, 2. Currently low-osmolar contrast media are used in approximately 75% of patients and the iso-osmolar contrast media, allegedly less toxic are becoming more popular 1. In spite of development of new contrast media, they still represent the third main cause of nosocomial-acquired acute renal failure (ARF) (10% of cases), substantially increasing hospitalization period, care costs and in-hospital morbi-mortality 3-6. The main goal is to address important aspects about the contrast-medium induced nephropathy (CMIN) that follows cardiac catheterization, including its definition, pathogenesis, incidence, risk factors, clinical picture, prevention, treatment and prognosis.
Contrast-induced encephalopathy (CIE) is an acute and reversible neurological disturbance associated with the intra-arterial administration of iodinated contrast medium during cardiac catheterisation. It may manifest with encephalopathy, motor and sensory disturbances; vision disturbances, including cortical blindness, ophthalmoplegia, aphasia; and seizures. Disruption of the blood-brain barrier and direct neuronal toxicity are believed to be implicated in the pathophysiology of the syndrome. Symptoms appear soon after contrast administration and resolve completely within 24-48 h. Risk factors may include hypertension, diabetes mellitus, renal impairment, the administration of large volumes of iodinated contrast, percutaneous coronary intervention or selective angiography of internal mammary grafts and previous adverse reaction to iodinated contrast. On cerebral imaging, CIE may mimic subarachnoid haemorrhage or cerebral ischaemia, but imaging may be normal. Prognosis is excellent with supportive management alone. CIE may recur, but re-challenge with iodinated contrast without adverse effects has been documented. CIE is a diagnosis of exclusion and is an important clinical entity to consider in the differential diagnosis of stroke following cardiac catheterisation. Physicians should be aware of it and consider it prior to initiating thrombolysis.
BackgroundAcute coronary obstruction following transcatheter aortic valve replacement (TAVR) is an uncommon but life-threatening event.Case summaryA 78-year-old man developed acute left main obstruction following transfemoral TAVR with a balloon-expandable valve. Cardiac arrest ensued, requiring emergent peripheral cardiopulmonary bypass. Percutaneous coronary intervention (PCI) to the left main coronary artery was performed with one drug-eluting stent. Intravascular ultrasound (IVUS) demonstrated focal underexpansion of the stent in its proximal segment which was not responsive to high-pressure non-compliant balloon dilatation, suggesting stent compression from either valve strut or calcific native leaflet. Therefore, to increase radial strength of the scaffolding at the site of compression, we deployed a second stent within the first stent, and further expanded that segment with high-pressure balloon inflations. Final IVUS demonstrated better expansion of the focally compressed segment. Following PCI, left ventricular function normalized completely. The patient was discharged from hospital on Day 3 post-procedure. At 12 weeks follow-up, his dyspnoea had improved significantly, and follow-up transthoracic echocardiography demonstrated normal left ventricular systolic function and normal aortic valve function.DiscussionEstablished risk factors for coronary ostial occlusion include a short distance between the aortic annulus and the coronary ostia (<10 mm) and a narrow aortic root (<28 mm at the sinuses of Valsalva). These two factors increase the likelihood that the native valve leaflets are displaced over and obstruct the coronary ostia when the aortic bioprosthesis is deployed. Perplexingly, our patient did not present with any of the recognized risk factors for acute coronary occlusion, suggesting other factors might be at play. We suggest that a leaflet length to coronary sinus height ratio greater than 1 might be an additional useful predictor of coronary occlusion during TAVR. In addition, we suggest that if residual focal stent compression from either valve strut or calcific leaflet exists after stent deployment and the latter is resistant to balloon dilatation, deploying a second concentric layer of stent might improve the radial strength of the scaffolding and improve overall stent expansion.
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