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Arterial hypertension is the most prevalent cardiovascular risk factor worldwide. Despite the availability of many and effective antihypertensive medications, the prevalence of uncontrolled blood pressure (BP) remains high. As sympathetic hyperactivity has long been recognized as a major contributor to resistant hypertension, catheter-based renal denervation (RDN) has emerged as a new strategy to reduce BP. RDN aims to interrupt the activity of renal sympathetic nerves by applying radiofrequency (RF) energy, ultrasound (US) energy, or injection of alcohol in the perivascular space. The Symplicity HTN-3 trial, the largest sham-controlled trial using the first-generation RF-based RDN device, failed to significantly reduce BP. Since then, new devices and techniques have been developed and consequently many sham-controlled trials using second-generation RF or US-based RDN devices have demonstrated the BP lowering efficacy and safety of the procedure. A multidisciplinary team involving hypertension experts, interventionalists with expertise in renal interventions and anesthesiologists, plays a pivotal role from the selection of the patient candidate for the procedure to the post-procedural care. The aim of this consensus document is to summarize the current evidence about the use of RDN in difficult to treat hypertension and to propose a management strategy from the selection of the patient candidate for the procedure to the post-procedural care.

Left ventricular hypertrophy is accompanied by the remodeling of the collagen network. We have studied collagen network in left ventricular hypertrophy secondary to aortic stenosis by cardiac catheterization and endomyocardial biopsies. We have demonstrated that collagen architecture is abnormal in 2/3 of patients with aortic stenosis and is more important than collagen concentration in influencing myocardial stiffness and ejection fraction. Furthermore, we observed that relaxation and asynchrony were influenced by the degree of hypertrophy instead of by the collagen network. The postoperative regression of left ventricular hypertrophy and the changes in interstitial tissue after valve replacement have been studied in a subgroup of patients. The major finding is that the regression of myocardial hypertrophy is a process that occurs over many years after correction of primary hemodynamic abnormality. Six to 7 years after valve replacement we observed, together with the normalization of diastolic stiffness, the complete normalization of interstitial fibrosis that was primarily increased (both pre and early postoperatively).

The purpose of this study was to evaluate left ventricular (LV) structure-function interplay in aortic stenosis. LV structure was assessed from endomyocardial biopsies obtained in 27 patients with aortic stenosis. Total collagen volume fraction, orthogonal collagen fiber meshwork (cross-hatching) and endocardial fibrosis were determined by morphologic-morphometric evaluation. Control biopsy data were obtained from 6 pre-transplantation donor hearts whereas other 11 patients with normal cardiac function served as hemodynamic controls. LV biplane cineangiography and high-fidelity LV pressure measurement were carried out in all patients. Systolic function was assessed by LV biplane ejection fraction, diastolic function by time constant of relaxation, peak filling rates and passive elastic properties. Total collagen volume fraction (7.3 versus 1.6%, p < 0.01) as well as the degree of cross-hatching (1.7 versus 0.8 grade, p < 0.01) were significantly increased in patients with aortic stenosis with respect to controls. Endocardial fibrosis was present in 11/27 patients with aortic stenosis and in no patients of control group. In aortic stenosis in presence of increased total collagen volume fraction there were no changes in systolic and diastolic function, whereas in presence of changes in collagen architecture ejection fraction was depressed and passive elastic properties increased. In conclusion, in aortic stenosis, changes in collagen architecture are associated with altered systolic function and passive diastolic properties. The sole increase in total collagen volume fraction without a change in architecture leaves systolic and passive diastolic function unaltered. A prolongation of relaxation was present in aortic stenosis and appears to be mediated by muscle hypertrophy per se.

Animal experiments and clinical observation in humans have established a window of opportunity during which reperfusion after acute myocardial infarction may salvage myocardium. This time window was initially thought to be 3 to 4 hours from the onset of coronary occlusion, but it has been recently recognized in humans to be longer, at least 6 hours and possibly even longer. The longer time span for effective intervention was determined in several studies showing an increased survival rate as a consequence of the improvement in left ventricular function and the reduction of infarct sequels with late thrombolysis. Main mechanism by which late thrombolysis may lead to survival benefit seems to be infarct-related artery patency. However, other mechanisms have been postulated such as the positive influence on remodeling, electric stability and different effects due to the breakdown of systemic fibrinogen and the anticoagulant effect that this can produce. Regardless of which of these proposed mechanisms is responsible for reducing mortality in patients treated with late thrombolysis after myocardial infarction, the limitation of treating patients only within the 4- to 6-hour time window must be seriously reconsidered.

This describes our preliminary experience with percutaneous brachial approach for cardiac catheterization, by using 5 French (F) preformed catheters. Thirty patients (pts) were studied from the left arm (Group A) with a 5F sheath and 5F Judkins catheters and 30 from the right arm (Group B) with 5F sheath and 5F Amplatz catheters. Pigtail catheters (5F) were used for the left ventricular angiograms in all patients. In 10 patients arterial velocity signals and radial and ulnar artery blood pressures were monitored with the Doppler ultrasonic velocity detector before and immediately after each procedure, and 24 hours later. Arterial puncture was carried out successfully in each patient by using a 18-gauge Potts-Cournand needle. The puncture site was as close as possible to the ante cubital fossa where the artery is less mobile. Both coronary arteries were selectively opacified and the left ventricular angiography was done on every patient. The diagnostic quality of the angiograms was evaluated by the visual analogue scale and the results were not different from those obtained with the femoral approach in our catheterization laboratory. In 3 out of 30 pts in group B it was impossible to obtain a good left coronary opacification with Amplatz catheters for anatomical reasons, thus the right femoral approach was preferred. Brachial artery occlusion occurred in 1 patient from group B and needed surgical thrombectomy carried out to restore normal radial and ulnar pulses.(ABSTRACT TRUNCATED AT 250 WORDS)