{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T11:27:13Z","timestamp":1793359633952,"version":"4.5.0"},"reference-count":13,"publisher":"American Medical Association (AMA)","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Cardiol"],"published-print":{"date-parts":[[2023,10,1]]},"abstract":"<jats:sec><jats:title>Importance<\/jats:title><jats:p>The role of the coronary venous circulation in regulating myocardial perfusion and its potential in treating microvascular angina is unexplored.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>To evaluate whether an increase in coronary venous pressure modifies microvascular resistance in patients with microvascular angina.<\/jats:p><\/jats:sec><jats:sec><jats:title>Design, Setting, and Participants<\/jats:title><jats:p>This was a blinded, sham-controlled, crossover, randomized clinical trial that enrolled participants between November 2021 and January 2023. Participants for this physiology end point study were recruited from the Cardiology Center of the University of Medicine in Mainz, Germany. Patients with moderate\/severe angina pectoris (Canadian Cardiovascular Society class 2-4) due to microvascular dysfunction (as defined by the thermodilution-based index of microvascular resistance &amp;amp;gt;25 mm Hg \u00d7 s). Exclusion criteria were epicardial coronary disease, second- and third-degree atrioventricular block, severe valvular heart disease, cardiomyopathy, and pulmonary or kidney disease.<\/jats:p><\/jats:sec><jats:sec><jats:title>Intervention<\/jats:title><jats:p>Inflation of an undersized balloon placed in the cardiac coronary sinus (CS), hereafter referred to as <jats:italic>balloon<\/jats:italic> and the deflated balloon in the right atrium, referred to as <jats:italic>sham<\/jats:italic>. Measurements were performed at rest and during maximal coronary hyperemia. Both patients and final assessors were blinded to the randomization sequence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Main Outcomes and Measures<\/jats:title><jats:p>Hemodynamic parameters, including aortic (Pa) and distal (Pd) coronary pressure, coronary sinus pressure (Pcs), right atrial pressure (Pra), and the mean transit time (inverse of blood flow [Tmn]), were measured.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A total of 20 patients (median [IQR] age, 69 [64-75] years; 11 female [55.0%]) were included in the study. Two patients (10%) had diabetes, 6 (30%) had hypercholesterolemia, 15 (75%) had hypertension, and 3 (15%) were active smokers. The inflation of the CS balloon caused a significant increase in CS pressure at rest and during hyperemia (300% and 317% increase, respectively, compared with sham, both <jats:italic>P<\/jats:italic>\u2009&amp;amp;lt;\u2009.001), a decrease in hyperemic distal coronary pressure (median [IQR], sham: 92 [80-100] mm Hg; balloon: 79 [75-93] mm Hg; <jats:italic>P<\/jats:italic>\u2009=\u2009.01) and mean transit time (sham: 0.39 [0.23-0.62] s; balloon: 0.26 [0.17-0.46] s; <jats:italic>P<\/jats:italic>\u2009=\u2009.008). As a result, CS occlusion led to a decrease in both resting coronary resistance (median [IQR], sham: 59 [37-87] mm Hg \u00d7 s; balloon: 42 [31-67] mm Hg \u00d7 s; <jats:italic>P<\/jats:italic>\u2009=\u2009.005) and the primary end point hyperemic coronary resistance (mean [IQR], sham: 31 [23-53] mm Hg \u00d7 s; balloon: 14 [8-26] mm Hg \u00d7 s; <jats:italic>P<\/jats:italic>\u2009&amp;amp;lt;\u2009.001).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion and Relevance<\/jats:title><jats:p>Increased coronary venous pressure led to a reduction of microvascular resistances in patients with microvascular angina, a mechanism with potential implications for the therapy of this complex disease.<\/jats:p><\/jats:sec><jats:sec><jats:title>Trial Registration<\/jats:title><jats:p>ClinicalTrials.gov Identifier: <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/classic.clinicaltrials.gov\/ct2\/show\/NCT05034224\">NCT05034224<\/jats:ext-link><\/jats:p><\/jats:sec>","DOI":"10.1001\/jamacardio.2023.2566","type":"journal-article","created":{"date-parts":[[2023,8,23]],"date-time":"2023-08-23T15:34:33Z","timestamp":1692804873000},"page":"979","source":"Crossref","is-referenced-by-count":49,"title":["Coronary Venous Pressure and Microvascular Hemodynamics in Patients With Microvascular Angina"],"prefix":"10.1001","volume":"8","author":[{"given":"Helen","family":"Ullrich","sequence":"first","affiliation":[{"name":"Department of Cardiology, Cardiology I, University Medical Center Mainz, Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philipp","family":"Hammer","sequence":"additional","affiliation":[{"name":"German Centre for Cardiovascular Research (DZHK), Partnersite RheinMain, Mainz, Germany"},{"name":"Helios Kliniken Schwerin, Schwerin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maximilian","family":"Olschewski","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Cardiology I, University Medical Center Mainz, Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"M\u00fcnzel","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Cardiology I, University Medical Center Mainz, Mainz, Germany"},{"name":"German Centre for Cardiovascular Research (DZHK), Partnersite RheinMain, Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Javier","family":"Escaned","sequence":"additional","affiliation":[{"name":"Hospital Clinico San Carlos, Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tommaso","family":"Gori","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Cardiology I, University Medical Center Mainz, Mainz, Germany"},{"name":"German 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