Masami Nishino

Relationship between effects of statins, aspirin and angiotensin II modulators on high-sensitive C-reactive protein levels

Statins, aspirin and angiotensin II modulators (A II-M: angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type I receptor blockades) may have an anti-inflammatory effect, but the relationship between the effects of statins, aspirin and A II-M on high-sensitive C-reactive protein (hs-CRP) levels remains to be determined. We examined serum hs-CRP levels in consecutive patients with stable ischemic heart disease (IHD) (n=1231; 65+/-9 years; male/female, 927/304) and without IHD (n=226; 64+/-9 years; male/female, 117/109). Blood samples were collected on the day of catheterization. The hs-CRP levels were significantly higher in the IHD than in the non-IHD patients (0.32+/-0.52 vs. 0.24+/-0.29 mg/dl, P<0.05). Treatment with statins was associated with significantly lower hs-CRP levels in both groups (non-IHD, 0.17+/-0.14 vs. 0.26+/-0.31 mg/dl; IHD, 0.27+/-0.34 vs. 0.35+/-0.59 mg/dl; both P<0.05). hs-CRP levels were significantly lower only in IHD patients treated with A II-M than in those not treated with A II-M (0.28+/-0.34 vs. 0.34+/-0.58 mg/dl, P<0.05). Aspirin did not have any effect on the hs-CRP level in either group. The hs-CRP levels were significantly lower in IHD patients treated with statins and/or A II-M than those treated with neither statins nor A II-M (statin+/A II-M+, 0.28+/-0.29 mg/dl; statin+/A II-M-, 0.26+/-0.36 mg/dl; statin-/A II-M+, 0.28+/-0.37 mg/dl; statin-/A II-M-, 0.38+/-0.66 mg/dl; P<0.01). These results indicate that statins and A II-M, but not aspirin, in commonly used doses have an anti-inflammatory action as assessed by measurement of CRP levels in IHD patients.

Increased Angiotensin-Converting Enzyme Activity in Coronary Artery Specimens From Patients With Acute Coronary Syndrome

Background —Angiotensin-converting enzyme (ACE) inhibitors are effective in the secondary prevention of ischemic heart disease, but they do not reduce the rate of restenosis. Vascular ACE activity in the culprit coronary lesions of these patients, however, has never been quantified. Methods and Results —We measured the ACE activity of vascular tissue obtained by directional coronary atherectomy in patients with acute coronary syndrome (n=17) and in patients with stable ischemic heart disease (n=36), with and without restenosis. The ACE activity of the culprit coronary lesions was significantly increased in patients with acute coronary syndrome (0.87±0.12 nmol · min–1 · mg protein–1;P <0.01) but not in patients with ischemic heart disease with restenosis (n=11, 0.19±0.05 nmol · min–1 · mg protein–1) when compared with those patients with ischemic heart disease without restenosis (n=25, 0.20±0.05 nmol · min–1 · mg protein–1). There was no difference between the ACE activity of the coronary tissue of the in-stent (n=5) and stent-unrelated (n=6) restenosis patients (0.24±0.10 versus 0.15±0.04 nmol · min–1 · mg protein–1). Serum ACE activity did not differ significantly among the patients. Conclusions —The present study demonstrates increased ACE activity in culprit lesions in acute coronary syndrome, indicating that enhanced ACE activity is related to the causative mechanism of active coronary lesions.

Evaluation of thoracic aortic atherosclerosis by transesophageal echocardiography

Transesophageal echocardiography (TEE) provides excellent images of the thoracic aorta, which cannot be visualized by transthoracic echocardiography. The purpose of this study was to assess atherosis and sclerosis of the thoracic aorta by TEE, to evaluate the risk factors for atherosis and sclerosis, and to assess the relationship between the two components of atherosclerosis. The mean value of the maximum thickness of the intima-media complex in the six segments of the thoracic aorta (MIMC) was used as an index of atherosis, and the stiffness parameter beta was used as an index of sclerosis. The study population consisted of 88 Japanese patients. Multivariate analysis showed that age, low-density lipoprotein cholesterol (or apolipoprotein B), and diabetes mellitus were significantly and independently related to MIMC, whereas age and hypertension were related to the stiffness parameter beta. Both components of atherosclerosis demonstrated a significant although weak relationship. The risk factors for atherosis appear to differ from those for sclerosis in the thoracic aorta, so we should evaluate these two components of atherosclerosis separately. TEE is a useful method of assessing thoracic aortic atherosclerosis because both atherosis and sclerosis can be examined simultaneously.

Recovery of impaired left ventricular function in patients with acute myocardial infarction is predicted by the discordance in defect size on123I-BMIPP and201TI SPET images

A discrepancy between myocardial perfusion defect and wall motion abnormalities is frequently found early after coronary reperfusion in patients with acute myocardial infarction. The purpose of this study was to assess recovery of impaired left ventricular function by reference to the discordance in defect size between myocardial fatty acid uptake and myocardial perfusion using combined single-photon emission tomographic (SPET) imaging early after coronary perfusion therapy. In 37 patients with acute myocardial infarction, iodine-123 15(p-iodophenyl)-3(R, S)-methylpentadecanoic acid (BMIPP) and thallium-201 SPET scans were performed early after coronary reperfusion. A severity score was determined from the extent of the imaging defect with each tracer. Left ventricular wall motion score (WMS) and ejection fraction (EF) were obtained at admission and at 4 weeks after the onset of infarction. In 32 of the 37 patients, discordance in defect sizes delineated with the two SPET studies was found during the acute stage. The severity score for BMIPP was larger than that for201Tl during the acute stage (7.7±2.4 vs 4.4±2.5,P <0.001). There was a fair correlation between the severity score for BMIPP and WMS (r=0.82,P <0.0001), but a poor correlation between that for201Tl and WMS. The extent of discordance in severity scores between BMIPP and201Tl during the acute stage correlated well with the extent of the improvement in WMS (r=0.86,P <0.0001) and that of EF (r=0.85,P <0.0001). We conclude that the discordance in defect size on BMIPP and201TI SPET images during the acute stage of infarction is an early predictor of the viability of the myocardium at risk of infarction.

Time to recover from atrial hormonal, mechanical, and electrical dysfunction after successful electrical cardioversion of persistent atrial fibrillation

Although transient atrial dysfunction has been reported after electrical cardioversion of atrial fibrillation (AF), the difference in the time to recover from the atrial hormonal, mechanical, and electrical dysfunction has not been described. Thus, we evaluated the time course of recovery from atrial hormonal, mechanical, and electrical dysfunction after cardioversion in patients with nonvalvular AF. We attempted electrical cardioversion in 87 consecutive patients with nonvalvular AF that had persisted for > or =6 months, and in 24 patients (28%) with maintained sinus rhythm for > or =6 months. To evaluate atrial hormonal, mechanical, and electrical dysfunction in these 24 patients, we measured plasma concentration of atrial natriuretic peptide, the atrial peak velocity in transmitral flow, and the ratio of peak systolic-to-diastolic pulmonary venous flow (S/D ratio) using echocardiography, and the duration and the root mean voltage for the terminal 20 ms (LP20) of the filtered P wave using P-wave signal-averaged electrocardiography. Atrial natriuretic peptide rapidly returned to baseline within 1 day after cardioversion, and maintained these levels for 6 months. Atrial peak velocity in transmitral flow and S/D ratio were significantly increased at 2 weeks, and continued to increase until 1 month, and then reached a plateau. The duration and LP20 began to recover only 6 months after cardioversion. One to 3 years after conversion, the duration and LP20 had nearly reached a plateau, but the latter value remained below normal. In patients with nonvalvular AF of prolonged duration, recovery from atrial electrical dysfunction after sinus conversion took much longer than that from either atrial hormonal or mechanical dysfunction.

Evaluation of the Mitral Valve Leaflet Morphology after Mitral Valve Reconstruction with a Concept “Coaptation Length Index”

Abstract  Background: In clinical settings, information on morphology of mitral valve leaflet after mitral valve reconstruction is limited. Methods: Between January 1996 and June 2000, 36 underwent mitral valve repair for mitral regurgitation (MR). The etiology of mitral insufficiency was prolapse, dilated annulus, and ischemic. Ring annuloplasty was performed in all cases. Mitral valve short‐axis dimension (MVd), vertical distance between annular line and closing point (Vd), coaptation length (CL), coaptation length index (CL/MVd) were measured by the two‐dimensional transesophageal echocardiography for the present 11 cases. Results: In 11 cases, residual MR, using a scale from 0 to 4, was 0 in 5 patients, 1 in 4 patients, 2 in 2 patients whose etiology of regurgitation was cardiomyopathy. MVd and Vd decreased significantly (38.7 ± 6.2 to 27.0 ± 5.6 mm, 10.1 ± 7.7 to 6.5 ± 4.6 mm, respectively). CL and CLI increased significantly (6.4 ± 2.4 to 11.6 ± 4.6 mm, 0.16 ± 0.06 to 0.44 ± 0.21, respectively). Among those index, only CLI have a statistically significant negative correlation with the degree of residual MR. Conclusion: The mitral valve ring annuloplasty produce the morphologic change of mitral apparatus, especially the increase of CLI, which may be one of the main factors in regulation of regurgitation.

Does Stringent Restrictive Annuloplasty for Functional Mitral Regurgitation Cause Functional Mitral Stenosis and Pulmonary Hypertension

Background— It remains controversial whether restrictive mitral annuloplasty (RMA) for functional mitral regurgitation (MR) can induce functional mitral stenosis (MS) that may cause postoperative residual pulmonary hypertension (PH). Methods and Results— One hundred eight patients with left ventricular (LV) dysfunction and severe MR underwent RMA with stringent downsizing of the mitral annulus. Systolic pulmonary artery pressure (PAP) and mitral valve performance variables were determined by Doppler echocardiography prospectively and 1 month after RMA. Fifty-eight patients underwent postoperative hemodynamic measurements. Postoperative echocardiography showed a mean pressure half-time of 92±14 ms, a transmitral mean gradient of 2.9±1.1 mm Hg, and a mitral valve effective orifice area of 2.4±0.4 cm2, consistent with functional MS. Doppler-derived systolic PAP was 32±8 mm Hg, which correlated weakly with the transmitral mean gradient (&rgr;=0.23, P=0.02). Postoperative cardiac catheterization also showed significant improvements in LV volume and systolic function, pulmonary capillary wedge pressure, cardiac index, and systolic PAP; the latter was associated with LV end-diastolic pressure [standardized partial regression coefficient (SPRC)=0.51], pulmonary vascular resistance (SPRC=0.47), cardiac index (SPRC=0.37), and transmitral pressure gradient (SPRC=0.20). In a multivariate Cox proportional hazard model, postoperative PH (systolic PAP >40 mm Hg), but not mitral valve performance variables, was strongly associated with adverse cardiac events. Conclusions— RMA for functional MR resulted in varying degrees of functional MS. However, our data were more consistent with the residual PH being caused by LV dysfunction and pulmonary vascular disease than by the functional MS. The residual PH, not functional MS, was the major predictor of post-RMA adverse cardiac events.

Right Ventricular Apical Pacing Impairs Left Ventricular Twist as Well as Synchrony: Acute Effects of Right Ventricular Apical Pacing

BACKGROUND This study was designed to compare the rotation of the left ventricular (LV) apex and base, LV synchrony between LV apical and basal rotation, and LV twist, changing from intrinsic atrioventricular conduction to right ventricular apical (RVA) pacing. METHODS Thirty consecutive patients with sick sinus syndrome who had undergone DDD pacemaker implantation were studied. Changing from intrinsic atrioventricular conduction to RVA pacing, the acute effect on echocardiographic parameters, including LV rotation and twist and LV apical-basal rotation delay, was assessed. RESULTS During RVA pacing, values of peak rotation in the LV apex and base and LV twist were significantly lower than during intrinsic atrioventricular conduction (P=.007, P=.003, and P<.0001, respectively). Apical-basal rotation delay during RVA pacing was significantly longer than during intrinsic atrioventricular conduction (P=.02). CONCLUSIONS RVA pacing decreases apical and basal LV rotation and induces LV apical-basal rotation delay, resulting in impairment of LV twist.

Dobutamine stress echocardiography at 7.5 μg/kg/min using color tissue Doppler imaging M-mode safely predicts reversible dysfunction early after reperfusion in patients with acute myocardial infarction

Abstract Dobutamine stress echocardiography (DSE) is widely used to predict reversible left ventricular dysfunction, but evaluation by this method is subjective. The recently developed color tissue Doppler imaging (TDI) M-mode may permit objective and quantitative assessment of changes in wall motion induced by DSE. We tested the hypothesis that this new method can detect sensitively reversible dysfunction in the post–myocardial infarction setting. DSE with color TDI M-mode and conventional DSE were performed to predict reversible dysfunction in 53 patients at a mean of 3 days after infarction using 7.5 and 10 μg/kg/min of dobutamine. Follow-up regular echocardiography (4 weeks later) was used as the reference technique to define reversible dysfunction segments. To predict reversible dysfunction segments, the standard segmental wall motion score change on conventional DSE and the ratio of the segmental wall velocity difference at rest versus stress (7.5 and 10 μg/kg/min) on DSE with color TDI M-mode (7.5-TDI-M and 10-TDI-M, respectively) were used. With 7.5 μg/kg/min of dobutamine, the sensitivity for predicting reversible dysfunction using color TDI M-mode (7.5-TDI-M) was significantly higher than that of conventional DSE (89% vs 73%, p

A Case of Acute Myocardial Infarction Intracoronary Thrombosis in Two Major Coronary Arteries Due to Hormone Therapy

A fifty-four-year-old woman was admitted to the hospital for a sensation of tightness in the chest of one hours duration. She had undergone surgery for breast cancer two years previously and had been taking 30 mg of tamoxifen and 1200 mg of medroxyproges terone daily after surgery. Emergency coronary angiography on admission revealed thrombi in both the right coronary artery and the left anterior descending coronary artery. Tissue-type plasminogen activator was injected into both coronary arteries, resulting in diminution of thrombus size. Repeat coronary angiography on the next day disclosed no thrombus in either artery and no significant stenosis. Electrocardiographic and laboratory data indicated myocardial infarction. These findings strongly suggest that the combination hormone therapy altered the patients blood coagulability and played an important role in the formation of the intracoronary thrombi and subsequent acute myocardial infarction.