BACKGROUND: The randomized, sham-controlled RADIANCE-HTN (A Study of the Recor Medical Paradise System in Clinical Hypertension) SOLO, RADIANCE-HTN TRIO, and RADIANCE II (A Study of the Recor Medical Paradise System in Stage II Hypertension) trials independently met their primary end point of a greater reduction in daytime ambulatory systolic blood pressure (SBP) 2 months after ultrasound renal denervation (uRDN) in patients with hypertension. To characterize the longer-term effectiveness and safety of uRDN versus sham at 6 months, after the blinded addition of antihypertensive treatments (AHTs), we pooled individual patient data across these 3 similarly designed trials. METHODS: Patients with mild to moderate hypertension who were not on AHT or with hypertension resistant to a standardized combination triple AHT were randomized to uRDN (n=293) versus sham (n=213); they were to remain off of added AHT throughout 2 months of follow-up unless specified blood pressure (BP) criteria were exceeded. In each trial, if monthly home BP was ≥135/85 mm Hg from 2 to 5 months, standardized AHT was sequentially added to target home BP <135/85 mm Hg under blinding to initial treatment assignment. Six-month outcomes included baseline- and AHT-adjusted change in daytime ambulatory, home, and office SBP; change in AHT; and safety. Linear mixed regression models using all BP measurements and change in AHT from baseline through 6 months were used. RESULTS: Patients (70% men) were 54.1±9.3 years of age with a baseline daytime ambulatory/home/office SBP of 150.5±9.8/151.0±12.4/155.5±14.4 mm Hg, respectively. From 2 to 6 months, BP decreased in both groups with AHT titration, but fewer uRDN patients were prescribed AHT ( P =0.004), and fewer additional AHT were prescribed to uRDN patients versus sham patients ( P =0.001). Whereas the unadjusted between-group difference in daytime ambulatory SBP was similar at 6 months, the baseline and medication-adjusted between-group difference at 6 months was −3.0 mm Hg (95% CI, −5.7, −0.2; P =0.033), in favor of uRDN+AHT. For home and office SBP, the adjusted between-group differences in favor of uRDN+AHT over 6 months were −5.4 mm Hg (−6.8, −4.0; P <0.001) and −5.2 mm Hg (−7.1, −3.3; P <0.001), respectively. There was no heterogeneity between trials. Safety outcomes were few and did not differ between groups. CONCLUSIONS: This individual patient-data analysis of 506 patients included in the RADIANCE trials demonstrates the maintenance of BP-lowering efficacy of uRDN versus sham at 6 months, with fewer added AHTs. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifiers: NCT02649426 and NCT03614260.
Abstract Background Coronary functional testing to formally diagnose coronary microvascular dysfunction (CMD) reduces cardiovascular events and alleviates angina. This study aims to investigate the extensive and complex journey that patients with CMD undergo, from the onset of chest pain to eventual diagnosis. Methods Data from the Coronary Microvascular Disease Registry (CMDR) were analyzed, including information on the date of first documentation of chest pain, number of non-invasive and invasive tests the patient underwent, emergency department visits, and hospitalizations. In addition, we estimated the total cost per patient. A total of 61 patients with CMD diagnosis were included in this analysis. Results The cohort had an average age of 65.6±9.9 years. The median time from initial chest pain symptoms to diagnosis was 0.62 (interquartile range [IQR]: 0.06-2.96) years. During this period, patients visited the emergency department a median of 1.0 (IQR: 0.0-2.0) times. Diagnostic tests included 3.0 (IQR: 2.0-6.0) electrocardiograms, 3.0 (IQR: 0.0-6.0) high-sensitivity troponin tests, and 1.0 (IQR: 1.0-2.0) echocardiograms. Prior to diagnosis of CMD, 13 (21.3%) patients had left heart catheterization without coronary functional testing. Non-invasive testing for ischemia was conducted in 43 (70.5%) patients. Alternative non-cardiac diagnoses were given to 11 (18.0%) patients during the diagnostic process, with referrals made to gastroenterology for 16 (26.2%) and pulmonology for 10 (16.4%) patients. The cost averaged $1,790±2,506 per patient. Conclusion Timely identification of CMD offers promising opportunities for prompt symptom alleviation, accompanied by reduced visits to the emergency department, cardiovascular testing, invasive medical procedures, and consequently reduced healthcare expenses. Clinical Trial Registry Coronary Microvascular Disease Registry (CMDR), clinicaltrials.gov , NCT05960474 What is Known; What the Study Adds What is Known - Angina pectoris is a major global health concern, impacting millions of individuals around the world. - Coronary microvascular dysfunction (CMD) is a known etiology to cause angina. What the Study Adds - This study reveals the challenging journey of CMD patients from chest pain to diagnosis, showing the complexity, and overlapping symptoms of CMD, leading to under/misdiagnosis or delay in definitive diagnosis. - Healthcare providers must improve CMD awareness and understanding to ensure timely and accurate diagnosis, minimizing patient burden and unnecessary expenses. - Further research and awareness campaigns are crucial to optimize CMD management, leading to better healthcare outcomes and reduced economic strain.
Physiological assessment of myocardial bridging prevents unnecessary interventions. Non-invasive workup or visual coronary artery compression may underestimate the underlying ischaemia associated with myocardial bridging in symptomatic patients.A 74-year-old male presented to the outpatient clinic with chest pain and shortness of breath on exertion. He underwent coronary artery calcium scan showing an elevated calcium score of 404. On follow-up, he endorsed progressive worsening of symptoms with chest pain and decreased exercise tolerance. He was then referred for coronary angiography that revealed mid-left anterior descending myocardial bridging with initial normal resting full-cycle ratio of 0.92. Further workup after ruling out coronary microvascular disease demonstrated abnormal hyperaemic full-cycle ratio of 0.80 with a diffuse rise across the myocardial bridging segment on pullback. Our patient also had increased spastic response to hyperaemia on angiography, supporting the presence of underlying endothelial dysfunction and ischaemia, likely contributing to his exertional symptomology. The patient was started on beta-blocker therapy with improvement in symptoms and resolution of chest pain on follow-up.Our case highlights the importance of thorough workup of myocardial bridging in symptomatic patients to better understand the underlying physiology and endothelial function after ruling out microvascular disease and consideration of hyperaemic testing if symptoms are suggestive of ischaemia.
