Association between the Red Cell Distribution Width and Vasospastic Angina in Korean Patients

PURPOSE: The association between the red cell distribution width (RDW) and vasospastic angina (VSA) has not been elucidated. We investigated the association of the RDW with the incidence and angiographic subtypes of VSA in Korean patients. MATERIALS AND METHODS: A total of 460 patients who underwent intracoronary ergonovine provocation tests were consecutively enrolled and classified into two groups: the VSA group (n=147, 32.0%) and non-VSA group (n=313, 68.0%). The subjects were classified into 3 subgroups (tertiles) according to the baseline level of RDW assessed before the angiographic provocation test. RESULTS: The VSA group had a higher RDW than the non-VSA group (12.9±0.8% vs. 12.5±0.7%, p=0.013). The high RDW level demonstrated an independent association with the high incidence of VSA [second tertile: hazard ratio (HR) 1.96 (1.13-2.83), third tertile: HR 2.33 (1.22-3.47), all p<0.001]. Moreover, the highest RDW tertile level had a significant association with the prevalence of the mixed-type coronary spasm [HR 1.29 (1.03-1.59), p=0.037]. CONCLUSION: The high level of RDW was significantly associated with the prevalence of VSA and the high-risk angiographic subtype of coronary spasm, suggesting that a proactive clinical investigation for VSA could be valuable in Korean patients with an elevated RDW.

An Increased Monocyte Count Predicts Coronary Artery Spasm in Patients with Resting Chest Pain and Insignificant Coronary Artery Stenosis

BACKGROUND: Coronary atherosclerosis with inflammation gives rise to coronary vasospasm in the patients with coronary vasospastic angina. We have postulated that the peripheral leukocyte count and the differential count are associated with vasospastic angina. METHODS: 144 patients who underwent intracoronary ergonovine provocation testing between January 2002 and December 2004 were divided into two groups: Group I (72 patients with provoked spasm, mean age: 54.8+/-10.7 years, males: 75%) and Group II (72 without spasm, mean age: 55.3+/-10.2 years, males: 35%). Blood sampling was done to measure the lipid profiles and inflammatory markers, including the high sensitive C-reactive protein (hsCRP) levels and the monocyte counts. We compared the angiographic findings and laboratory data between the two groups. RESULTS: There were no significant differences in the levels of serum lipid and hsCRP between the two groups. The white blood cell count and the monocyte count were higher in Group I than with Group II (7496.4+/-2622.28 vs. 6703.2+/-1768.37/mm3, respectively, p=0.035; 627.5+/-270.70 vs. 426.9+/-205.76/mm3, respectively, p<0.001). Gensini's score was higher in Group I than in Group II (2.2+/-2.88 vs. 0.5+/-1.03, respectively, p<0.001). Multivariate analysis showed that the monocyte count and Gensini's score were independent factors affecting coronary spasm (p=0.047 and p=0.018, respectively). According to a receiver operating characteristics curve analysis, the area under the curve of the monocyte count was 0.738, that of the neutrophil count was 0.577 and that of the WBC count was 0.572. The cut-off value of the monocyte count was 530/mm3; the sensitivity and specificity of this cut-off value were 64% and 76%, respectively. CONCLUSIONS: The peripheral monocyte count is an independent marker for predicting vasospastic angina in the patients with resting chest pain and insignificant coronary artery stenosis.

A study of platelet aggregation, thromboxane A2 and prostacyclin in central aortic and coronary sinus blood in ischemic heart disease.

Aortic and coronary sinus platelet aggregation, thromboxane A2 (TXA2) and prostacyclin (PG12) levels were studied in fourteen patients of stable angina (SA), six of vasopastic angina (VA) and six control subjects (C). Patients of SA were studied at rest and during incremental atrial pacing and patients with VA were studied at rest and during various stages of vasospasm. Platelet aggregation was studied with different working concentrations of ADP, epinephrine and collagen. TX A2 and PGI2 concentrations were estimated by measuring levels of their stable metabolites viz. thromboxane B2 (TXB2) and 6-keto prostaglandin F1 alpha (PGF1 alpha) respectively. Platelet aggregation was increased in SA and VA patients (p < 0.01) and further increase was seen during vasospasm (p < 0.001). However, it failed to increase on incremental atrial pacing. Similarly, TXB2 and PGF1 alpha levels were raised in SA and VA patients. While TXB2 further increased during vasospasm but not during atrial pacing. PGF1 infinity failed to rise with either. Thus platelets are in an activated state in SA and VA. This activated state is a cause and not an effect in SA and VA. An imbalance in the levels of TXA2 and PG12 could account for the vasospasm.