Katsuhiro Kawaguchi

Quantitative estimation of infarct size by simultaneous dual radionuclide single photon emission computed tomography: Comparison with peak serum creatine kinase activity

To test the hypothesis that simultaneous dual energy single photon emission computed tomography (SPECT) with technetium-99m (99mTc) pyrophosphate and thallium-201 (201TI) can provide an accurate estimate of the size of myocardial infarction and to assess the correlation between infarct size and peak serum creatine kinase activity, 165 patients with acute myocardial infarction underwent SPECT 3.2 +/- 1.3 (SD) days after the onset of acute myocardial infarction. In the present study, the difference in the intensity of 99mTc-pyrophosphate accumulation was assumed to be attributable to difference in the volume of infarcted myocardium, and the infarct volume was corrected by the ratio of the myocardial activity to the osseous activity to quantify the intensity of 99mTc-pyrophosphate accumulation. The correlation of measured infarct volume with peak serum creatine kinase activity was significant (r = 0.60, p less than 0.01). There was also a significant linear correlation between the corrected infarct volume and peak serum creatine kinase activity (r = 0.71, p less than 0.01). Subgroup analysis showed a high correlation between corrected volume and peak creatine kinase activity in patients with anterior infarctions (r = 0.75, p less than 0.01) but a poor correlation in patients with inferior or posterior infarctions (r = 0.50, p less than 0.01). In both the early reperfusion and the no reperfusion groups, a good correlation was found between corrected infarct volume and peak serum creatine kinase activity (r = 0.76 and r = 0.76, respectively; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Intravascular ultrasound-guided percutaneous coronary intervention for total occlusion of the proximal left anterior descending artery caused by spontaneous coronary dissection in a young woman

A 35-year-old woman was admitted to our hospital because of a sudden cardiac arrest caused by an acute anterior myocardial infarction. Emergency coronary angiography showed total occlusion of the proximal left anterior descending artery (LAD). We performed an intravascular ultrasound (IVUS) to detect the LAD orifice and successfully inserted the guidewire to the occluded LAD. An IVUS revealed coronary dissection and no atheromatous plaque from the orifice to the mid-portion of the LAD and the guidewire was in the true lumen. Two bare metal stents were implanted in the proximal and mid portion of the LAD. After stenting to the LAD, coronary dissection retrogradely extended to the left circumflex artery (LCx). Therefore, we performed additional stent implantation from the left main trunk (LMT) to the proximal LCx and the just proximal LAD. An IVUS guided percutaneous coronary intervention (PCI) enabled complete revascularization to spontaneous coronary artery dissection.

Pull-down maneuver of stent graft for abdominal aortic aneurysm with accessory renal arteries

A 78-year-old man admitted to our hospital because of Stanford B type acute thoracic aortic dissection. CT imaging showed abdominal aortic aneurysm (AAA) and bilateral common iliac arterial aneurysms (Fig. 1a, b). He also had bilateral accessory renal arteries (Fig. 1c). The length from the lower accessory renal artery to the terminal aorta was 63 mm. Although his anatomical structure was not suitable for endovascular aortic aneurysm repair (EVAR), we thought it possible to accomplish EVAR, because the length of neck below the lower renal artery was 24 mm and the neck was not so bending, which was enough for sealing neck with stent graft. We performed embolization of internal iliac arteries and EVAR 6 months later. We selected Gore® Excluder® AAA endoprosthesis system, whose length from the top of the stent graft to the end of the contralateral gate is 80 mm. When we deployed the stent graft below the lower accessory renal artery as the conventional method, the contralateral gate would locate in the ipsilateral common iliac artery. On the other hand, if we push up the contralateral gate above the bifurcation, the lower renal arteries would be sacrificed (Fig. 1d). Therefore, we tried to pull down the stent graft once deployed above the renal arteries. We inflated the balloon within the contralateral limb of the stent graft, and constrained the proximal trunk (Fig. 1e). Then, we simultaneously pulled down the main body and the inflated balloon catheter till the top of the stent graft was positioned below the lower renal artery. Final angiography showed the intact lower renal arteries and no endoleak into the aneurysm (Fig. 1f). Accessory renal artery is an anatomical variation found in 28–30% of the general population [1]. The presence of an accessory renal artery arising from the seal zone or aneurysm requires coverage by the stent graft or embolization during EVAR, and it may cause renal function deterioration. Renal infarction occurred only in patients with accessory renal arteries, and 14% of eGFR decreased in 1 week after EVAR, while no renal infarction was observed in patients without accessory renal arteries [2]. When the length of neck below the lower renal artery was enough and the neck was not so bending, we can expect good result of EVAR with pull-down maneuver for patients with accessory renal arteries.

Myocardial Isoenzyme Distribution in Chronic Diabetes: Comparison with Isoproterenol-Induced Chronic Myocardial Damage

In the chronically diabetic heart, it has been reported that the activity of several enzymes bound to cell structures, such as sarcoplasmic reticular Ca++ ATPase, sarcolemmal Na+-K+ ATPase and myosin ATPase is depressed and that the isoenzyme distribution of myosin ATPase is altered (1,2). However, the changes in the activity and isoenzyme distribution of creatine kinase (CK: EC 2.7.3.2) and lactate dehydrogenase (LD: EC 1.1.1.27) which are mainly “soluble” enzymes and clinically important markers of myocardial necrosis (3) have not been reported in the diabetic heart previously. Therefore, in this study we measured total and isoenzyme activities of myocardial CK and LD in rats with insulin dependent diabetes and compared them with control. Since intracellular calcium overload has been suggested in the pathogenesis of diabetic cardiomyopathy (1,2,4), we also measured the activity of the same (iso)enzymes in the myocardium of rats chronically injected with isoproterenol, a pure s-adrenergic stimulant, which develop cardiomyopathy with intracellular calcium overload (5).