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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.

Monocytes and high-density lipoprotein cholesterol (HDL-C) play important roles in the process of coronary atherosclerosis. We hypothesized that a reasonable predictive model of coronary plaque regression might be constructed using the change in the peripheral monocyte count and the serum HDL-C level. The plaque volume, as assessed by volumetric intravascular ultrasound, was measured at the baseline and after 6 months of pravastatin therapy in 114 patients with coronary artery disease. After 6 months of pravastatin therapy, a significant decrease of the plaque volume by 9.9% (p 0.0001, vs. baseline) was observed; furthermore, a corresponding increase of the serum HDL-C level and decrease of the peripheral blood monocyte count were also seen (12.5%, p 0.01 and -7.3%, p 0.0001). In a multivariate regression analysis using the serum lipids and traditional risk factors as the covariates, the increase in the serum HDL-C (β -0.56, p 0.0001) and the decrease in monocyte count (β 0.23, p = 0.03) were identified as independent predictors of the plaque regression. A model for the prediction of plaque regression according to whether the achieved the change in (Δ) monocyte count and ΔHDL-C were above or below the median values was prepared. Among the four groups, the group with ΔHDL-C ≥8.8% and Δmonocyte count ≤-8.6% showed the largest plaque regression (-20.4%), and the group with ΔHDL-C8.8% and Δmonocyte count-8.6% showed the increase of the plaque volume (2.6%). In view of the inflammatory nature of atherosclerosis, the model constructed using the two predictors may be a useful model for the prediction of plaque regression.

Low density lipoproteins (LDLs) are heterogeneous aggregations of molecules of different particle sizes, and small-size LDLs are more potent risk factors for atherosclerosis. We examined the qualitative characteristics of LDLs in patients with stable coronary artery disease (CAD) receiving statin therapy. LDL-particle size was estimated based on the LDL-cholesterol/apolipoprotein B ratio (LDL-C/apoB) in 214 age-adjusted men receiving statin therapy. The LDL-C/apoB ratio was significantly lower in the CAD (+) group (n = 107) than in the CAD (-) group (n = 107) (median, 1.17 versus 1.19, P = 0.0095). LDL-C/apoB was significantly lower in patients with serum TG ≥ 150 mg/dL than in those with serum TG < 150 mg/dL, and in patients with serum HDL-C < 40 mg/dL than in those with serum HDL-C ≥ 40 mg/dL (1.06 versus 1.18, P = 0.012; 1.08 versus 1.22, P = 0.0023). Stepwise logistic regression analysis revealed that elevated serum TG was an independent predictor for smaller sizes of LDLs, both in the overall subjects (β : -0.165, P = 0.02) as well as in the subset with serum LDL-C < 100 mg/dL (β : -0.252, P = 0.011). This study demonstrated that not only the absolute serum LDL-C level, but also the qualitative characteristics of LDL may be monitored for secondary prevention of CAD. Such monitoring is particularly important in patients with elevated serum TG levels, which is associated with smaller sizes of LDL-particles.

Heart failure after acute myocardial infarction (AMI) is an important factor in determining clinical outcome. We examined whether the plasma homocysteine level was a predictor of heart failure in patients with AMI. A series of 96 patients without renal failure who were admitted to our hospital because of AMI between January 2003 and December 2005 were assigned to two groups; a group with a high homocysteine level (group H: n = 48) and a group with a low homocysteine level (group L: n = 48) based on a median homocysteine level. Congestive heart failure was defined as Killip Class II or higher at the time of admission or the development of congestive heart failure after hospitalization. The mean brain natriuretic peptide (BNP) level at the time of admission in group H was higher than that of group L (175.3 pg/mL versus 89.9 pg/mL; P = 0.068). The incidence of heart failure in group H was significantly higher than that in group L (43.7% versus 12.5%; P < 0.001, log-rank test; hazard ratio: 2.92). Multivariate Cox regression analysis indicated that a high plasma homocysteine level of 10.8 µmol/L or higher was a risk factor for the development of heart failure (HR: 7.175, P < 0.01). The plasma homocysteine level in patients with AMI may be related to the development of heart failure.

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% (p0.0001 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 p0.0001, respectively, vs baseline), a significant increase of 14.0% of and 12.0% in the level of apoA-I and apoA-II (both p0.0001 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.

The purpose of this study was to clarify the relation between differential leukocyte counts and inhibition of the development of coronary atherosclerosis in patients with coronary artery disease. A 6-month prospective study was conducted in 84 patients treated with pravastatin. Plaque volume, as assessed by volumetric analysis using intravascular ultrasound, decreased significantly by 12.6% (p0.0001 vs baseline) after treatment; furthermore, a corresponding decrease of total leukocyte count (8.9%, p0.01 vs baseline) was seen. Change in plaque volume was correlated with changes in monocyte (r = 0.35, p = 0.002) and lymphocyte (r = 0.25, p = 0.03) counts but not with changes in neutrophil, eosinophil, or basophil counts. In a multivariate regression analysis with changes in serum lipids, traditional risk factors, and medications as covariates, the decrease in monocyte count was identified as an independent predictor of coronary plaque regression (beta coefficient 0.313, 95% confidence interval 0.089 to 0.353, p = 0.0014). No correlation was found between change in monocyte count and changes in any other lipid levels. This study demonstrated that monocyte count was the only leukocyte type significantly and independently associated with coronary atherosclerotic regression, even after adjustment for changes in any lipid levels. In conclusion, the decrease in monocyte count as a nonlipid-lowering effect of statins may be used as a novel marker of coronary atherosclerotic regression.

While the usefulness of measuring the plasma levels of brain natriuretic peptide (BNP) in cases with worsening heart failure and severe heart failure has already been established, the benefits of evaluation of this parameter in asymptomatic stable patients with left ventricular dysfunction is still under debate. Left ventricular function was evaluated in 141 ambulatory outpatients with a previous history of myocardial infarction not associated with symptoms of heart failure for at least one year. The plasma BNP level was also determined in these patients for comparative study. No correlation between the plasma level of BNP and EF was noted in the normal-EF group, while a negative correlation between the two parameters was observed in the low-EF group (Y = 0.439 - 0.000266X) (R2 = 0.244, P < 0.0001). The sensitivity was 91.5%, specificity 56.3%, positive predictive accuracy value 61.9%, and negative predictive accuracy value 83.8% for a plasma BNP cut-off level of 89.0 pg/mL. The results suggested that it might be meaningful to measure the plasma BNP level, especially in asymptomatic patients with a previous history of myocardial infarction having a low-EF.

Heart failure after acute myocardial infarction (AMI) is an important factor in determining clinical outcome. We examined whether the plasma homocysteine level was a predictor of heart failure in patients with AMI. A series of 96 patients without renal failure who were admitted to our hospital because of AMI between January 2003 and December 2005 were assigned to two groups; a group with a high homocysteine level (group H: n = 48) and a group with a low homocysteine level (group L: n = 48) based on a median homocysteine level. Congestive heart failure was defined as Killip Class II or higher at the time of admission or the development of congestive heart failure after hospitalization. The mean brain natriuretic peptide (BNP) level at the time of admission in group H was higher than that of group L (175.3 pg/mL versus 89.9 pg/mL; P = 0.068). The incidence of heart failure in group H was significantly higher than that in group L (43.7% versus 12.5%; P0.001, log-rank test; hazard ratio: 2.92). Multivariate Cox regression analysis indicated that a high plasma homocysteine level of 10.8 µmol/L or higher was a risk factor for the development of heart failure (HR: 7.175, P0.01). The plasma homocysteine level in patients with AMI may be related to the development of heart failure.