Toshiyuki Oniki

Alcohol and Coronary Spasm

Alcohol is known to sometimes cause coronary spasm, the mechanism of which is still unknown. The authors monitored changes in plasma levels of prostanoids (thromboxane [TX B 2], 6-keto prostaglandin F1α [PGF1α]), catecholamines (CA), serotonin (5-HT), cyclic nucleotides (cyclic adenosine monophosphate—cAMP, cyclic guanosine monophosphate— cGMP), and platelet aggregation after alcohol ingestion (Japanese rice wine 400 mL) in 8 patients with alcohol-induced variant angina and 8 healthy men as controls. Coronary spasm was confirmed to have been induced in 4 patients nine hours after alcohol challenge (VA[+]), when their plasma ethanol levels had already returned to a null level. Neither CA nor 5-HT levels showed any change after alcohol ingestion either in patients or controls, though controls showed high levels of CA during alcohol ingestion. TX B2 in VA (+) patients increased gradually after alcohol ingestion to reach up to a statistically signifi cantly high level just before attack, as compared with those of controls and VA(-) patients, who, on the contrary, did not show such changes. The levels of 6-keto PGF1α, however, which were significantly lower in patients than in controls before the test, exhibited a gradual increase in VA (+) patients in parallel with the increase in TX B2. No significant changes in cAMP levels between either controls or patients were present. On the contrary, cGMP levels had a gradual decrease in patients after alcohol ingestion. Especially six hours after alcohol ingestion, cGMP levels in VA (+) patients decreased so much as to make a statistically significant difference, as compared with the level in controls. Platelet aggregability in controls showed a decrease after alcohol ingestion, in spite of no change or even increase in patients. These data suggest that low levels of PGF1α and the decrease of cGMP levels from alcohol ingestion play important roles in the mechanism of coronary spasm induced by alcohol ingestion.

Thallium-201 stress scintigraphy in Takayasu arteritis

Thirty-eight women with Takayasu arteritis were studied using thallium-201 stress myocardial scintigraphy to assess the prevalence and pathophysiology of the perfusion abnormality. Twenty (53%) had abnormal scintigraphic findings (group A). Abnormal scans were divided into 3 groups: permanent defects in 6, reversible defects in 7 and slow washout in 7. The remaining 18 patients had normal scintigrams (group N). Group A had a tendency to be older and to have a high prevalence of complicated significant aortic regurgitation. Interventricular thickness plus left ventricular posterior wall thickness (26 +/- 7 vs 17 +/- 2 mm, p less than 0.01) and left ventricular mass (267 +/- 121 vs 133 +/- 39 g, p less than 0.01) were all greater in group A on echocardiography. The mean value of the central aortic pressure in systole was 170 +/- 15 mm Hg in the 7 catheterized patients in group A. Coronary ostial stenoses were present in 2 group A patients who showed reversible defects on scintigrams. These data indicate that the abnormal perfusion detected by imaging in patients with Takayasu arteritis was responsible for a decrease in coronary reserve or myocardial damage, or both, due to long-standing systemic hypertension or aortic regurgitation. Coronary artery disease should be considered if a reversible defect is present.

Aortic regurgitation in patients with Takayasu arteritis: assessment by color Doppler echocardiography.

SummaryTo characterize aortic regurgitation in patients with Takayasu arteritis, we studied 48 females with arteritis (mean age 47 ± 12 years) by means of color Doppler echocardiography. Aortic regurgitation was confirmed in 32 out of 48 patients (67%) by colorflow mapping. Twenty-four patients had mild or no aortic regurgitation (group A), 9 had moderate (group B), and 15 had severe (group C) aortic regurgitation. We compared the echocardiographic data obtained from patients with Takayasu arteritis with those of 14 normal controls and 9 patients with severe aortic regurgitation of valvular origins (group V). The aortic root diameter (AOD) in group B (23 ± 4 mm/M2) and group C (22 ± 3 mm/M2) revealed a statistically significant large value as compared with that in group A (18 ± 2 mm/M2) and normal controls (17 ± 3 mm/M2). However, the differences, between groups B and C and groups C and V, were not significant. The AOD was not obviously dilated in a considerable number of group C patients. Aortic valve involvement was seen in several group C patients and moderate concentric left ventricular hypertrophy was present in all group C patients. Group C patients therefore, have concentric left ventricular hypertrophy but may or may not have dilatation of the aortic root which can be detected on echocardiography. We conclude that aortic valve involvement may cause aortic regurgitation in some patients with Takayasu arteritis and that aortic regurgitation is more common than previously believed.

Left Ventricular Geometry in Takayasu Arteritis Complicated by Severe Aortic Regurgitation

Although it has been reported that the aortic regurgitation (AR) of patients with Takayasu arteritis is due to dilatation of the aortic ring, the geometry of the left ventricle (LV) has not been described. We compared the cardiac findings in patients with Takayasu arteritis (TA) and severe AR with those of patients having severe AR of other origins. Echocardiographically, wall thickness (WT) and the concentric hypertrophic ratio (WT/WT + left ventricular end-diastolic dimension) were greater in patients with TA. It is concluded that the LV of the TA patients revealed concentric hypertrophy even when AR was severe.

Is arterial remodeling truly a compensatory biological reaction?: A mechanical deformation hypothesis

It has been recognized that arterial enlargement occurs in relation to the formation of atherosclerotic plaque. Previous studies on arterial remodeling have disregarded the role of mechanical deformation and have suggested that compensatory mechanisms occur to maintain arterial flow. We postulated that primary atherosclerotic enlargement and mechanical deformation are the predominant causes of the arterial remodeling. This hypothesis better explains the morphological changes without suggesting additional biological reactions.

Enhanced flow velocity increase through the left ventricular inflow tract of patients with isolated aortic regurgitation

Twenty-five patients with chronic aortic regurgitation (AR), and 12 control subjects were studied using Doppler echocardiography to investigate the effects of AR on transmitral flow. Peak early filling velocities at the levels of the mitral valve tips (E1) and annulus (E2) were measured, and the transmitral flow restriction index (delta E = (E1-E2)/E2) was obtained. Patients with AR were classified into 2 groups according to the ratio of the cross-sectional area of the regurgitant jet to that of the left ventricular outflow tract. Group I had the ratio less than 0.20, and group II had greater than or equal to 0.20. E2 in group II was lower than in control subjects, whereas E1 was not significantly different in any groups. delta E in group II was higher than in group I or in control subjects (p less than 0.05 and 0.01, respectively). delta E showed a significant correlation with the cross-sectional area ratio in all patients with AR (r = 0.70, p less than 0.01) and in group II (r = 0.82; p less than 0.01). Our data suggest that AR restricts early transmitral filling, and that delta E may indicate the increased driving pressure caused by flow restriction and is a useful hemodynamic index of AR.

Effects of Dobutamine on Left Ventricular Diastolic Performance Are Attenuated in Patients With Systemic Hypertension

We measured Doppler echocardiographic diastolic parameter during infusion of low-dose dobutamine in 14 untreated hypertensive subjects and in 14 normal controls. Low-dose dobutamine accelerated left ventricular relaxation in normal controls but not in hypertensive subjects.

Concentric Left Ventricular Hypertrophy in Patients with Takayasu Arteritis

Although aortic regurgitation (AR) in patients with Takayasu arteritis (TA) is believed to be caused by dilatation of the aortic ring or thickening of the aortic cusps, the pattern of left ventricular hypertrophy (LVH) in these patients has not been described. To clarify the geometry of the LV in patients with TA that had been documented both echocardiographically and hemodynamically, the authors evaluated 22 patients with TA and severe AR (group 1), 10 with TA and systemic hypertension (group 2), and 17 with isolated severe AR of other etiolo gies (group 3). M-mode echocardiography showed that LV dimensions were smaller in groups 1 and 2 than in group 3 and that wall thickness was greater in group 1 than in group 3. The concentric hypertrophic ratio (CHR = wall thick ness/LV end-diastolic dimension + wall thickness) was larger than group 1 (p < 0.001) and group 2 (p < 0.01) than in group 3. CHR was similar in groups 1 and 2. Systolic blood pressure was significantly increased in group 2 and showed a tendency to increase in group 1 as compared with group 3. The results confirmed the presence of concentric LVH related to a pressure overload in patients with TA, even when TA was complicated by severe AR.

Ethanol Modulates Cyclic GMP Metabolism in Cultured Coronary Smooth Muscle Cells

The authors tested the hypothesis that ethanol or its metabolite acetaldehyde might interfere in cyclic guanosine monophosphate (GMP) metabolism in coronary smooth muscle cells. Ethanol at the physiologically relevant concentration of 4.0 mg/mL or more significantly decreased basal guanylate cyclase activity and inhibited activation of the enzyme by sodium nitroprusside (SNP) in cultured porcine coronary smooth muscle cells. Two isoforms of phosphodiesterase (PDE), cyclic GMP-specific form and calmodulin-stimulated form, were both inhibited by 12.0 mg/mL or more ethanol. Intact cell study revealed that although 12.0 mg/mL or more ethanol was needed to significantly decrease cyclic GMP accumulation in control cells, 4.0 mg/mL or more ethanol significantly inhibited the increase of cyclic GMP accumulation induced by 1 μm SNP. Acetaldehyde showed similar effects, but the concentrations involved were more than physiological. Thus, ethanol may decrease cellular cyclic GMP levels and attenuate cyclic GMP accumulation in response to SNP in coronary smooth muscle cells by inhibiting soluble guanylate cyclase activity at physiologically relevant concentrations.

Transesophageal Echocardiographic Recognition of a Fistula Between a Coronary Artery and the Left Atrium

A 58-year-old woman with a prosthetic mitral valve and an anomalous single coronary artery received transesophageal echocardiography and was found to have a coronary artery--to--left atrium fistula. Because of its superior imaging quality, transesophageal color Doppler method is a useful diagnostic procedure.