TY - JOUR
T1 - Coronary microvascular dysfunction and cancer therapy-related cardiovascular toxicity
AU - Chitturi, Kalyan R.
AU - Bhogal, Sukhdeep
AU - Kassaian, Seyed Ebrahim
AU - Merdler, Ilan
AU - Abusnina, Waiel
AU - Chaturvedi, Abhishek
AU - Ben-Dor, Itsik
AU - Waksman, Ron
AU - Case, Brian C.
AU - Barac, Ana
AU - Hashim, Hayder D.
N1 - Publisher Copyright:
© 2024
PY - 2024
Y1 - 2024
N2 - Background: Coronary microvascular dysfunction (CMD) has been implicated as a potential mechanism in the pathophysiology of different clinical presentations, including ischemia and no obstructive coronary artery disease (INOCA), myocardial infarction and nonobstructive coronary arteries (MINOCA), stress cardiomyopathy, heart failure, and myocarditis. There are limited data about the role of CMD in cancer therapy-related cardiovascular toxicities. Case presentations: Four women with a diagnosis of active cancer receiving treatment who developed subsequent MINOCA or INOCA presented for cardiac catheterization. Upon coronary angiography showing no obstructive coronary arteries, coronary function testing was performed to evaluate for CMD. Methods: Coronary physiology was assessed measuring non-hyperemic (resting full-cycle ratio [RFR]) and hyperemic (fractional flow reserve [FFR]) indices using a physiologic pressure wire. The wire also measured coronary flow reserve (CFR), index of microcirculatory resistance (IMR), and RFR using thermodilution technology. CMD was confirmed if the CFR was <2.5 and the IMR was >25. Results: Among 4 patients with diagnosis of active cancer presenting with chest pain, there was no evidence of obstructive coronary artery disease, leading to separate diagnoses of INOCA, MINOCA, stress cardiomyopathy, and myocarditis. We found CMD in 2 patients (1 with INOCA and 1 with immune checkpoint inhibitor-related myocarditis). Conclusions: CMD may play a role in cardiovascular toxicities. Further coronary physiology studies are needed to understand the mechanisms of cancer therapy-related cardiovascular toxicity and CMD, as well as optimal preventive and treatment options.
AB - Background: Coronary microvascular dysfunction (CMD) has been implicated as a potential mechanism in the pathophysiology of different clinical presentations, including ischemia and no obstructive coronary artery disease (INOCA), myocardial infarction and nonobstructive coronary arteries (MINOCA), stress cardiomyopathy, heart failure, and myocarditis. There are limited data about the role of CMD in cancer therapy-related cardiovascular toxicities. Case presentations: Four women with a diagnosis of active cancer receiving treatment who developed subsequent MINOCA or INOCA presented for cardiac catheterization. Upon coronary angiography showing no obstructive coronary arteries, coronary function testing was performed to evaluate for CMD. Methods: Coronary physiology was assessed measuring non-hyperemic (resting full-cycle ratio [RFR]) and hyperemic (fractional flow reserve [FFR]) indices using a physiologic pressure wire. The wire also measured coronary flow reserve (CFR), index of microcirculatory resistance (IMR), and RFR using thermodilution technology. CMD was confirmed if the CFR was <2.5 and the IMR was >25. Results: Among 4 patients with diagnosis of active cancer presenting with chest pain, there was no evidence of obstructive coronary artery disease, leading to separate diagnoses of INOCA, MINOCA, stress cardiomyopathy, and myocarditis. We found CMD in 2 patients (1 with INOCA and 1 with immune checkpoint inhibitor-related myocarditis). Conclusions: CMD may play a role in cardiovascular toxicities. Further coronary physiology studies are needed to understand the mechanisms of cancer therapy-related cardiovascular toxicity and CMD, as well as optimal preventive and treatment options.
KW - cancer
KW - Coronary microvascular dysfunction
KW - Ischemia and no obstructive coronary artery disease
KW - Myocardial infarction and nonobstructive coronary arteries
UR - http://www.scopus.com/inward/record.url?scp=85194100438&partnerID=8YFLogxK
U2 - 10.1016/j.carrev.2024.05.001
DO - 10.1016/j.carrev.2024.05.001
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C2 - 38789343
AN - SCOPUS:85194100438
SN - 1553-8389
JO - Cardiovascular Revascularization Medicine
JF - Cardiovascular Revascularization Medicine
ER -