Can the premises of the spasm of resistance vessel concept permit improvement in the treatment and prevention of ischemic heart disease?
In this communication, the spasm of resistance vessel (S-RV) concept of ischemic heart disease (IHD) and other ischemic will be reviewed and updated, and evidence will be presented that principles of the hypothesis might improve the treatment and prevention of IHD. The S-RV concept provides a different basic pathogenetic framework for IHD, and suggestions for treatment and prevention stem from its different basic conceptualization of this disorder. The concept asserts that S-RV directly induces symptoms in IHD, and this position challenges the accepted pathogenetic mechanism for this disorder, i.e., that symptoms in IHD are due directly to obstructive occlusions of epicardial arteries secondary to coronary artery disease. The S-RV concept avers that ischemia-induced S-RV is a major factor in IHD, and evidence supporting this position is provided. Another major position of the hypothesis is that no-reflow (reduced flow after infarction and severe myocardial ischemia in the absence of infarction) is due to ischemic injury-induced S-RV, and a variety of evidences to support this position are offered.Proposed improvement in the treatment of IHD is based mainly on treating ischemia-induced S-RV. alpha-Adrenergic sympathetic blockade reverses ischemia-induced S-RV, and alpha-adrenergic blockade is suggested as therapy for acute coronary syndromes and to prevent complications of percutaneous coronary interventions. Also, angiotensin-converting enzyme inhibition, which has actions similar to alpha-adrenergic blockade, is also suggested. Proposals for the prevention of IHD are based the prevention of S-RV, and special emphasis is given to preventing exercise- and stress-related IHD.
Hellstrom
H R
HR
Department of Pathology, College of Medicine, SUNY Upstate Medical University, Syracuse, NY 13210, USA. hellstrr@mail.upstate.edu
D000208:Acute Disease; D000787:Angina Pectoris / Q000503:physiopathology; D001792:Blood Platelets / Q000502:physiology; D003328:Coronary Thrombosis / Q000150:complications / Q000503:physiopathology; D003329:Coronary Vasospasm / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control* / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000503:physiopathology; D012307:Risk Factors; D013577:Syndrome; D014655:Vascular Resistance / Q000502:physiology*