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- H.Richard Hellstrom, MDa
I read with interest the study by Sun et al. (1), which showed that 25.5% of patients with vasospastic angina developed myocardial ischemia with submaximal doses of intracoronary acetylcholine; angina was unassociated with spasm of epicardial arteries and was attributed to microvascular spasm. Remaining patients developed myocardial ischemia only when epicardial spasm occurred, and Sun et al. (1) did not rule out the coexistence of microvascular spasm in these cases.
The Sun et al. (1) study is in keeping with the spasm of resistance vessel (S-RV) concept of ischemic heart disease (IHD) (2–5), which asserts that S-RV induces symptoms in all syndromes of IHD and in cases with and without coronary artery disease (CAD). S-RV is used instead of microvascular spasm, as spasm probably occurs in vessels designed to undergo vasomotion to maintain vascular homeostasis. The concept asserts that risk factors act additively and operate by favoring S-RV, and there is evidence that major risk factors favor S-RV—including hypercholesterolemia and CAD (2,4,5). The concept avers that stenotic CAD favors S-RV through ischemia-induced S-RV, and there is abundant evidence that significant ischemia favors S-RV (2,5). As an example, effort angina is attributed to stenotic CAD plus exertion, which together cause sufficient ischemia to trigger ischemia-induced S-RV and clinical symptoms.
Interest in S-RV in IHD has been limited mainly to vasospastic angina, as these cases are unassociated with stenotic CAD. But there is evidence for S-RV in stable angina (3,5), and relative insufficiency probably is an invalid mechanism; cholesterol- and stress-reduction significantly improved angina in a month’s time (6), long before CAD could be improved—a finding incompatible with classic relative insufficiency (3,5). Favorable to the concept, cholesterol reduction favors vasodilation and can improve vasodilation in one month (7) and, as stress can cause S-RV (3), stress-reduction reasonably is vasodilative. Also, while plaque rupture/thromboses are the accepted mechanisms of acute coronary syndromes, a recent analysis showed significant faults with this mechanism (5). For example, studies of infarction showing rising incidences of thromboses over time are incompatible with primary thromboses. If thromboses cause infarction, how can their incidence increase over time? And recognition of S-RV during ischemic episodes in unstable angina (8) is consistent with the S-RV cause of this angina.
The S-RV concept offers an explanation for the only occasional occurrence of vasospastic angina, and a viable explanation should help establish the reasonableness of the concept. As vasospastic angina is unassociated with CAD, this major vasoconstrictive force is absent, and angina occurs only when there are high levels of other risk factors as stress, gender and genetic factors, etc.—which occur only occasionally. In IHD associated with CAD, symptoms are attributed to the risk factor of CAD plus other risk factors such as stress; consistent with this, induced stress can cause myocardial ischemia in individuals with stable angina (9,10). Also, absence of IHD in many individuals with severe CAD is explained by the relative absence of other risk factors such as stress.
Although considerable evidence supports the standard position, there appears to be sufficient contravening evidence for the S-RV concept to prompt a comprehensive review of its positions.
- American College of Cardiology Foundation
- O’Driscoll G.,
- Green D.,
- Taylor R.R.
- Marzilli M.,
- Sambuceti G.,
- Fedele S.,
- L’Abbate A.