Shingo Furuya

Treatment of coronary spastic angina with a statin in addition to a calcium channel blocker: a pilot study.

Combined therapy with a statin and a calcium channel blocker, which can improve lipid metabolism and reduce oxidative stress, may attenuate coronary vasoconstriction in patients with coronary spastic angina (CSA). After 6 months of therapy with benidipine and pravastatin, an acetylcholine provocation test was performed a second time in 25 patients with CSA. The patients were divided into 2 groups according to whether the result of this second test was positive (n = 13) or negative (n = 12). The test was designated as positive when the intracoronary injection of acetylcholine induced angiographically demonstrable total or subtotal occlusion (positive-test group). In the negative-test group, significant decrease in the plasma levels of low-density lipoprotein (LDL) cholesterol (−20.7 ± 11.1%, P < 0.01 versus baseline) were observed along with a dramatic increase in the serum level of high-density lipoprotein (HDL) cholesterol (26.8 ± 13.2%, P < 0.01 versus baseline). Furthermore, a significant decrease of the malondialdehyde-modified low-density lipoprotein (MDA-LDL) level, a marker of oxidative stress, was also observed (-22.6 ± 14.1%, P < 0.01 versus baseline) in this group. In the positive-test group, however, no significant changes were found in any of the aforementioned parameters. The results showed that improvement of lipid metabolism, especially an increase of HDL cholesterol level and a reduction of MDA-LDL, may inhibit vascular contractility.

Association of plasma level of malondialdehyde-modified low-density lipoprotein with coronary plaque morphology in patients with coronary spastic angina: implication of acute coronary events.

BACKGROUND Focal vasospasm is reportedly involved in a high incidence of acute coronary syndrome (ACS) as compared with diffuse vasospasm. No adequate studies have been conducted on the mechanism underlying the higher incidence of ACS involving focal vasospasm than of those involving diffuse vasospasm in patients with coronary spastic angina. METHODS AND RESULTS Blood samples were collected from the aortic root (Ao) and the coronary sinus (CS) before provoking left coronary vasospasm using intracoronary administration of acetylcholine. After relief of vasospasm, volumetric analyses of vasospastic lesions were evaluated with 3-dimensional intravascular ultrasound in 64 patients. The percent plaque volume was more prominent in focal (n=31) than in diffuse vasospasm (n=33) (40.9+/-9.4 vs. 23.3+/-9.2%, p<0.0001). The Cs-Ao difference of malondialdehyde-modified low-density lipoprotein (MDA-LDL) level, as a marker of atherothrombosis, in focal vasospasm increased significantly as compared with diffuse vasospasm (6.9+/-6.7 vs. 1.2+/-5.7 U/L, p=0.001). In a multiple-logistic regression analysis with the traditional risk factors, the Cs-Ao difference of MDA-LDL level was a variable differing independently between the 2 types of vasospasm. CONCLUSIONS Higher MDA-LDL levels were observed in the coronary circulation in patients with focal vasospasm than in those with diffuse vasospasm. Under these conditions, the dramatically increased percent plaque volume in cases with focal vasoconstriction may play an important role in the development of acute coronary events.

Relation of change in apolipoprotein B/apolipoprotein A-I ratio to coronary plaque regression after Pravastatin treatment in patients with coronary artery disease.

Some investigations have looked into the ability of measurements of apolipoprotein B/apolipoprotein A-I (apoB/apoA-I) ratio to predict cardiovascular events. We hypothesized that a decrease in the apoB/apoA-1 ratio by statin therapy would act on suppression of coronary plaque progression. A 6-month prospective study was conducted of 64 patients with coronary artery disease treated with pravastatin. The plaque volume, assessed by volumetric intravascular ultrasonography, had decreased significantly by 12.6% (p <0.0001 vs baseline). Although a significant decrease of 6.4% and 14.6% was found in the serum level of apoB and the apoB/apoA-1 ratio (p = 0.0001 and p <0.0001, respectively, vs baseline), a significant increase of 14.0% of and 12.0% in the level of apoA-I and apoA-II (both p <0.0001 vs baseline). No significant changes were found in the level of apoC-II or apoE. A stepwise regression analysis revealed that the change in the apoB/apoA-1 ratio was an independent predictor of the change in coronary plaque volume (beta coefficient 0.386; p = 0.0023). In conclusion, our results have indicated that the decrease in the apoB/apoA-I ratio is a simple predictor for coronary atherosclerotic regression: the lower the apoB/apoA-I ratio, the lower the risk of coronary atherosclerosis.

Efficacy of Calcium Channel Blocker in the Secondary Prevention of Myocardial Infarction

BACKGROUND Calcium channel blockers (CCBs) may have a positive influence on the long-term prognosis of Japanese patients with ischemic heart disease. METHODS AND RESULTS The effect of nifedipine-retard (NR) (n=202) compared with that of non-CCB treatment (n=92) on the secondary prevention of myocardial infarction (MI) was retrospectively investigated in patients who had survived acute MI between 1987 and 1996. The primary endpoint was the occurrence of cardiac death or non-fatal MI. The median follow-up was 6.3+/-2.4 years. The incidence of cardiac events was 8.9% in the NR group and 14.1% in the non-CCBs group (p=0.14, odds ratio (OR): 0.584, 95% confidence interval (CI): 0.286-1,193). However, subanalysis revealed that NR significantly reduced the incidence of cardiac events in patients aged less than 55 years (4.2 vs 18.2%, p=0.016, OR: 0.180, 95%CI: 0.045-0.721) and those who did not smoke (8.6 vs 16.4%, p=0.048, OR: 0.462, 95%CI: 0.203-0.999). CONCLUSION Although this was a retrospective analysis, it showed that NR did not cause an increase in the incidence of cardiac events in post-MI patients; it even prevented cardiac events, especially in those who were less than 55 years of age and in non-smokers, suggesting the potential usefulness of CCBs in the secondary prevention of MI in Japan.

Takotsubo cardiomyopathy in two patients with microvascular angina

We present two cases in which takotsubo cardiomyopathy (TC) developed immediately after a diagnosis of microvascular angina had been established. One patient who had been diagnosed as having endothelium-dependent microvascular angina (microvascular spasm) developed TC three weeks after the initial admission. The other patient was diagnosed as having endothelium-independent microvascular angina (decreased coronary flow reserve) and subsequently developed TC after the discontinuation of nicorandil treatment. These cases may provide insight into the possible mechanisms underlying the pathophysiological findings of TC. <Learning objective: Impaired coronary microcirculation has been recently reported in many cases during the acute phase of takotsubo cardiomyopathy. However, the exact mechanism responsible for the coronary microvascular dysfunction associated with this entity remains unclear. This report highlights the importance of microvascular angina, which may play a role in the development of this cardiomyopathy.>.

Decreased coronary blood flow velocity in two patients with coronary microvascular spasm: case series†

Abstract Introduction Diagnostic criteria for coronary microvascular spasm (CMS) have not yet been fully established. Case presentation We present two cases of CMS in which decreased coronary blood flow velocities were observed during acetylcholine (ACH) provocation tests. The first patient suffered from chest pain occurring while at rest. The patient underwent coronary angiography (CAG), which revealed a decrease in the average peak velocity (APV) from 29 cm/s to 14 cm/s and a slow flow phenomenon following ACH injection. The second patient suffered from chest pain occurring during the night. The patient underwent CAG, which revealed a decrease in the APV from 17 cm/s to 7 cm/s with no significant epicardial coronary artery spasm following ACH injection. Both patients complained of chest pain, and electrocardiogram changes were observed in leads equivalent to the distal area of the vessel during an ACH provocation test. These findings were consistent with CMS, and their conditions improved under medical treatment. Discussion A transient decrease in coronary blood flow velocity following ACH administration might be a phenomenon specific to CMS. These cases may provide some insight into the underlying pathophysiology of CMS.

Complete occlusion of the left main trunk coronary artery by a cardiac papillary fibroelastoma in a hemodynamically unstable patient

Papillary fibroelastomas are benign cardiac tumors with high embolic potential. The majority of cases of complete obstruction of the left main trunk (LMT) of the coronary artery are diagnosed via autopsy following sudden death; survival is rare in this setting. We present the case of a 60-year-old woman who underwent stent placement in the LMT three years prior to developing chest pain and cold sweats. On coronary arteriography, the catheter could not be advanced into the LMT due to resistance in the ostium. Insertion of the catheter was achieved after the resolution of resistance via catheterization of the LMT by means of an intra-aortic balloon pump drive system. The LMT was normal, and the patients circulatory failure improved. The cause of the LMT embolism was a cardiac papillary fibroelastoma. Primary surgical excision is the recommended therapy for symptomatic cardiac papillary fibroelastoma. If the patient is hemodynamically stable, it may be possible to delay surgery. However, the patient in question developed cardiogenic shock secondary to two-vessel obstruction by the tumor. Therefore, even if the tumor had been removed using an intra-aortic balloon pump, the patient may not have survived until surgery. <Learning objective: Primary surgical excision is the recommended therapy for symptomatic cardiac papillary fibroelastoma. If the patient is hemodynamically stable, it may be possible to delay surgery. However, hemodynamically unstable patients may not survive until surgery. Therefore, emergent therapy is a useful stop-gap measure until surgery is feasible.>.