How to turn veins into arteries, without the surgery

SCIENCE AND MEDICINE

How to turn veins into arteries, without the surgery new non-surgical technique reported this week may provide a future alternative to coronary artery bypass surgery. The technique, known as percutaneous in-situ coronary venous arterialisation (PICVA), involves connecting a coronary vein to a coronary artery that has been blocked, thus bypassing the blockage with minimal surgery (Circulation 2001; 103: 2539–42). “One of the most invasive things you can do in medicine is coronary artery bypass surgery”, says Stephen Oesterle (Massachusetts General Hospital, Harvard Medical School, MA, USA). “Our ultimate goal is to replace traditional coronary artery bypass with a procedure that does not require surgery.” An international

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team performed the procedure in November, 1999, in Germany on a 53-year-old man who had one heart artery blocked almost its entire length by atherosclerosis. The patient is now living a normal, pain-free life. The investigators specifically targeted a patient who was not eligible for bypass surgery or balloon angioplasty because his artery was too severely blocked. During PICVA, an ultrasoundguided catheter system is inserted into an artery in one leg, and pushed up the aorta into the coronary arteries. Guided by ultrasonography, a hole is made into a vein adjacent to the blocked artery, held open with a stent, and blood is re-routed. After the procedure, blood flows in reverse to oxygenate the heart muscle, rather

than following the normal course of the vein up into the heart’s pumping chambers. “The technique described in this report is ingenious”, says Timothy Gardner (University of Pennsylvania Medical Center, PA, USA). “This report, however, describes short-term success in only one patient whose PICVA treatment was used in only one blocked artery. The vast majority of coronary artery patients who require angioplasty or bypass surgery need to have multiple blockages opened or bypassed.” Further, he warns that this technique must be proven safe and effective for patients, and durable over many years. Sally Hargreaves

Stress and education level linked to stroke risk in middle-aged men

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Science Photo Library

tress is linked to increased risk induced blood pressure reactivity of stroke in middle-aged white and subsequent 11-year risk of men says a new stroke. study. Susan Everson Men who had above Rights were not (University of Michmedian systolic blood granted to include igan, MI, USA) and pressure spikes (⭓20 colleagues, measured mm Hg) had a 72% this image in the reaction to stress greater risk of any electronic media. in 2303 white middlestroke compared with Please refer to the aged men by comparmen with less reactive printed journal. ing resting blood blood pressures. Men pressure with readwho were poorly eduings taken before an cated and had high exercise tolerance blood pressure reactest a week later. tivity were nearly MRI scan of a stroke They used data from three times more the Kuopio Ischemic likely to have a stroke Heart Disease risk factor study to than better educated men with less assess the relation between stressreactive blood pressures. Adjust-

ment for stroke risk factors had little impact on these associations (Stroke 2001; 32: 1263–69). “We believe these findings indicate that the health effects of physiologic tendency to react strongly to stress are compounded by the difficult life circumstances associated with low levels of education”, said co-worker George Kaplan. But, Larry Goldstein (Duke Center for Cerebrovascular Disease, NC, USA) cautions that “it remains to be established whether treatments to blunt the reactive blood pressure response reported here would decrease the risk of stroke”. Minal Chande

Akt2-deficient mice show symptoms of type 2 diabetes ice that lack the gene for Akt2, the phosphoinositide-dependent serine-threonine protein kinase, develop a syndrome similar to type 2 diabetes, report US researchers this week, indicating that Akt2 has a role in the insulin signalling pathway. Akt2 has been suggested to have a role in mediating the action of insulin, but results so far have been contradictory. “Several years ago we became attracted to Akt as a potential mediator of insulin action in muscle and fat, and others have postulated a role in liver”, explains researcher Morris Birnbaum (Howard Hughes Medical Institute and the University of Pennsylvania, Philadelphia, PA, USA). “We have argued in the past

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THE LANCET • Vol 357 • June 2, 2001

for the importance of Akt2 in metabolic signalling, and therefore generated mice deficient in the expression of this isoform.” The researchers found that insulin’s ability to suppress glucose production was completely abolished in mice lacking the Akt2 gene. The mice also had reduced disposal of glucose following administration of insulin (Science 2001; 292: 1728–31). The study shows that “Akt2 is critical to normal insulin signalling, and thus brings us one step closer to mapping the entire pathway”, says Birnbaum. Jan Erik Henriksen (Odense University Hospital, Denmark) stresses that the findings do not indicate that a lack of Akt2 causes

diabetes. “This study does not prove that a human defect in the Akt2 gene is responsible for the development of type 2 diabetes”, he says, “but does indeed suggest that defects distal in the insulin signalling cascade lead to insulin resistance in mice and therefore needs to be tested in every aspect in humans.” Robert Heine (Vrije Universiteit Medical Center, Amsterdam, the Netherlands) described the study as “interesting” but questioned what the implications were for ␤-cell function. “Perhaps the potential impact on ␤-cell function should be examined in the next study”, he suggested. Helen Frankish

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