Key result
Angiographic arterial waves are observed in various arteries, with an incidence of approximately 3% in femoral and renal arteriograms, and debated etiologies including spasm or standing waves.
This review discusses the incidence and proposed physical and biological mechanisms of angiographic arterial waves.
Angiographic arterial waves may be incidental findings; leaves open questions on etiology and clinical relevance.
Wave-like changes in arterial contours which do not correspond to pathologic alterations at the sites in the vessel where they occur are sometimes observed on arteriograms. Typically, the waves are regular in appearance and approximately sinusoidal. They may be present on one occasion and not on another, and they may be seen in different areas of the same vessel. The phenomenon has been given various descriptive names by different observers: “stationary arterial waves” (13, 21), “regular alternating changes in arterial width” (9), “beading” or “crenation” (17), “bamboo pattern” (22), “string of pearls” (11), “spasm simulating organic disease” (8), “contractions … during arteriography” (12), etc. These changes were first reported in the arteries of patients studied for occlusive disease of the lower extremities (21, 22). Later, similar changes were noted in renal, visceral, and iliac branches of the abdominal aorta (11, 12), as well as the carotid artery (13, 17). The incidence of arterial waves varies with the site being examined. It is highest in the femoral and renal arteries. Thus, in femoral arteriography one can derive a total incidence of 9/318, or approximately 3 per cent, by combining the figures of Theander—4 in 160, and Köhler—5 in 158. Meaney and Buonocore reported a similar 3 per cent incidence (19 of 600) in renal arteriograms. The phenomenon is considerably less frequent in the carotid artery; New, in a series of 2,000 arterio-graphic studies, reported its occurrence in 3 patients. Iliac and mesenteric arteries also appear to be less frequently affected than the femoral and renal, but reports have been too fragmentary to permit statistical evaluation. Explanations of the phenomenon of arterial waves have generally invoked either physical or biological mechanisms, usually in a mutually exclusive fashion. Wickbom and Bartley, citing a case in which the contractions disappeared after injection of the vasodilating drug Priscoline, concluded that the etiology was spasm. Theander critized this concept, noting that some arteries showing arterial waves actually appeared widened rather than narrowed. Theander made the further observation that arterial waves tended to occur in an area of slowed arterial flow, for example, proximal to an occlusion, embolus, or marked tortuosity. He suggested that the pulse wave was reflected to cause a standing wave pattern which, in favorable cases, would be further amplified by “resonance.” Köhler (9) rejected Theander's suggestion, stating that such oscillations would require physically unavailable amounts of energy, since the pulse wave would be damped out rapidly by “soft” arterial walls. He also contended that the wave lengths of observed arterial waves, in the order of several millimeters, were too short to be explained by reflected pulse waves which have been ascertained to have a wave length of several meters.
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Harold Lehrer (1967) conducted a review in Angiographic arterial waves. Angiographic arterial waves was evaluated. Angiographic arterial waves are observed in various arteries, with an incidence of approximately 3% in femoral and renal arteriograms, and debated etiologies including spasm or standing waves.
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