Sachie Akita

Effects of the Dietary Approaches to Stop Hypertension (DASH) Diet on the Pressure-Natriuresis Relationship

Abstract—Blood pressure-lowering mechanisms of the Dietary Approaches to Stop Hypertension (DASH) diet, rich in fruits, vegetables, and low-fat dairy foods, were analyzed based on the pressure-natriuresis relationship. Participants (n=375) were randomly assigned to control or DASH diet groups by using a parallel-group design. They then ate their assigned diet for 3 consecutive 30-day intervention feeding periods, during which sodium intake varied among 3 levels by a randomly assigned sequence. Urinary sodium excretion rate and mean arterial pressure were measured at the end of each sodium intake level. Mean arterial pressure and urinary sodium excretion were plotted on x and y axes, respectively, for participants eating control and DASH diets and were modeled as linear relationships for simplicity to allow the estimation of the extrapolated x-intercept and slope of the relationships. The DASH diet steepened the slope of the relationship (29.5±3.4 vs 64.9±13.1 [mmol/d]/mm Hg, P =0.0002) without significantly shifting the x-intercept (94.1±0.5 vs 93.2±0.6 mm Hg, NS) of the relationship. These data suggest a natriuretic action of the DASH diet.

Evaluation of left ventricular early diastolic performance by color tissue Doppler imaging of the mitral annulus

A noninvasive assessment of left ventricular (LV) diastolic performance by tissue Doppler imaging was performed in 56 patients (8 patients with atypical chest pain, 42 with coronary artery disease with a previous myocardial infarction, and 6 without a previous myocardial infarction) who underwent cardiac catheterization. Mitral annular velocity (MAV) during early ventricular diastole was obtained by M-mode color tissue Doppler imaging at the posterior corner of the mitral annulus. In each patient, the negative peak of the first derivative of LV pressure decay (peak -dP/dt) and a time constant of LV relaxation (tau) were calculated from the LV pressure waves obtained by a catheter-tip micromanometer. LV end-systolic volume index was measured from contrast left ventriculography. MAV during early diastole was significantly correlated with tau (r = -0.73, p <0.001), peak -dP/dt (r = 0.58, p <0.001), and LV end-systolic volume index (r = -0.63, p <0.001). On multivariate regression analysis with MAV during early diastole, tau and LV end-systolic volume index were selected as prime determinants (r = 0.80, p <0.001). These findings suggest that MAV during early diastole has a direct relation to LV elastic recoil as well as to LV relaxation. MAV during early diastole gives important information regarding LV behavior in late systole to early diastole where LV early diastolic performance is determined.

Takayasu's arteritis accompanied with massive pericardial effusion--a case report.

A 40-year-old woman who had been treated for Takayasus arteritis was admitted to the hospital with fever, fatigue, malaise, and severe chest pain. Computed tomography of the chest demonstrated massive pericardial effusion and bilateral pleural effusion. In laboratory data, the C-reactive protein was high at 22.0 mg/dL, and erythrocyte sedi mentation rate was also high at 80 mm/hr. The diagnosis was pericarditis with a recur rence of the systemic inflammatory process of Takayasus arteritis. The patient was treated with methylprednisolone pulse therapy. Her massive pericardial effusion disap peared without pericardiocentesis.

Left ventricular isovolumic relaxation flow and left ventricular systolic performance

We investigated isovolumic relaxation flow in patients with coronary artery disease (CAD) and evaluated the relationship between its velocity and left ventricular performance in 23 patients with atypical chest pain, 30 patients with CAD without prior myocardial infarction (MI), and 57 patients with prior MI, in whom cardiac catheterization was performed. The isovolumic relaxation flow velocity was measured at the basal portion of the left ventricle with pulsed Doppler echocardiography. The isovolumic relaxation flow ( > 15 cm/sec) was detected in 98 of 110 patients. The isovolumic relaxation flow velocity was significantly lower in patients with prior MI than in patients with atypical chest pain (p < 0.001) and in those with CAD without prior MI (P < 0.05). It was significantly lower in patients with CAD without prior MI than in those with atypical chest pain (p < 0.05). The isovolumic relaxation flow velocity showed a significant positive correlation with left ventricular ejection fraction. It also showed a significant negative correlation with left ventricular end-systolic volume index. These findings suggest that the isovolumic relaxation flow velocity is decreased in patients with CAD and is influenced by left ventricular systolic performance. Isovolumic relaxation flow may be a clinical manifestation of elastic recoil of the left ventricle.

Effects of volume loading on pulmonary venous flow pattern in dogs with normal left ventricular function

The effects of altered loading conditions on the pattern of pulmonary venous flow are poorly understood. The authors investigated such effects, therefore, by using volume loading in 6 open-chest dogs. The pulmonary venous flow volume rate curve was obtained with a transit-time ultrasonic flowmeter at a fixed heart rate. Measurements were performed in the control and several states during the intravenous infusion of dextran. The influences of volume loading on hemodynamic and pulmonary venous flow variables were compared between the control state and three interventional states in which mean left atrial pressure was approximately 1, 2, and 3 mm Hg above the control value. The systolic flow volume (SI), which corresponds to left atrial reservoir volume, significantly increased, but the early diastolic flow volume (DI), which corresponds to left atrial conduit volume, did not show significant change with volume loading. The flow volume during left atrial contraction significantly increased with volume loading. The flow volume during one cardiac cycle (PVF) significantly increased with volume loading. Approximately 73% of increased PVF was distributed to the systolic flow. The rest was distributed to the early diastolic flow (14%) and to the flow during left atrial contraction (12%). The change in the ratio of SI/DI significantly and positively correlated with the change in mean left atrial pressure (r=0.87, P < 0.001). These findings indicate that increased pulmonary venous flow induced by volume loading in dogs with normal left ventricular function is mainly distributed to the left atrial reservoir volume.

Comparative effects of volume loading on pulmonary venous flow in dogs with normal heart and with myocardial ischemia

The influences of cardiac loading conditions and left ventricular performance on pulmonary venous flow are poorly understood. The authors studied the effects of volume loading on the pattern of pulmonary venous flow in normal and ischemic hearts. Thirteen anesthetized dogs were equipped with a transit-time ultrasonic flow probe around the left upper pulmonary vein. In 6 of the dogs, the left anterior descending artery was ligated to induce myocardial ischemia. The remaining 7 dogs had normal hearts. Heart rate was fixed at 110 beats/minute by right atrial pacing. Dextran was infused from the femoral vein until mean left atrial pressure increased 3 mm Hg above the baseline value in both groups. In normal heart, systolic pulmonary venous flow volume (SI) increased significantly, but early diastolic flow volume (DI) did not show a significant change during volume loading. The ratio of SI/DI increased significantly (1.12 ±0.34 vs 2.11 ±0.49, P<0.05). After ligation of the left anterior descending artery, the SI and DI decreased significantly. The ratio of SI/DI did not show a significant change (0.88 ±0.32 vs 0.87 ±0.30, ns). In dogs with myocardial ischemia, volume loading caused increases in the SI and DI. However, no significant change was observed in the ratio of SI/DI (0.87 ±0.30 vs 0.97 ±0.36, ns). These findings demonstrate that left ventricular performance influences the alter ation in pulmonary venous flow pattern that is caused by systemic volume loading.

Paradoxical brain embolism caused by pulmonary arteriovenous fistula and coincident pulmonary embolism--a case report.

The authors encountered a very rare case of paradoxical brain embolism resulting from pulmonary arteriovenous fistula and coincident pulmonary embolism. Enhanced computed tomography was useful for diagnosing this infrequent condition.

Is the Blood Flow in the Left Ventricle during the Isovolumic Relaxation Period a Useful Parameter of Left Ventricular Systolic and Early Diastolic Performance

Left ventricular (LV) early diastolic performance is determined by LV behavior in the late systole to early diastole and may relate to the physical potential of patients. Isovolumic relaxation flow (IRF) velocity was obtained by continuous Doppler echocardiography in the left ventricle from the apex in 26 patients with atypical chest pain and 63 patients with coronary artery disease (CAD) with or without prior myocardial infarction (MI) who underwent cardiac catheterization. In each patient, a time constant of LV relaxation (τ) was calculated from the LV pressure waves obtained by a catheter-tipped micromanometer. The LV end-systolic volume index was measured using contrast left ventriculography. IRF velocity in patients having CAD with prior MI (24.8 ± 5.4 cm/s) was significantly less than in those with atypical chest pain (41.2 ± 9.6 cm/s). It was also significantly less than in patients having CAD without prior MI (37.3 ± 6.8 cm/s). IRF velocity significantly correlated with the time constant τ (r = –0.42, p < 0.001) and LV end-systolic volume index (r = –0.84, p < 0.001). This study indicates that IRF velocity obtained by continuous Doppler echocardiography in the left ventricle provides important information regarding LV systolic performance and early diastolic performance.

Estimation of Pulmonary Capillary Wedge Pressure from M-Mode Mitral Echograms

We investigated whether the isovolumic relaxation time (IRT) and an interval from the start of opening to the maximal amplitude of the anterior mitral leaflet in early diastole (D-E interval) would be useful predictors of the pulmonary capillary wedge pressure (PCWP). We recorded M-mode mitral echograms and phonocardiograms in 33 patients (aged 38-70 years) with acute myocardial infarction (AMI) in the coronary care unit and in 34 patients (aged 40-75 years) with prior myocardial infarction (OMI) during cardiac catheterization. All patients underwent the insertion of a flow-directed pulmonary artery catheter to obtain the PCWP. We measured the IRT and the D-E interval from the phonocardiograms and the M-mode echograms. There was no significant correlation between the IRT and the mean PCWP (mPCWP) in patients with AMI and in patients with OMI. The D-E interval was significantly and inversely correlated with the mPCWP (r = -0.91, p <0.0001) in all patients. The regression equation was mPCWP = -0.42 x (D-E) +47.9. The D-E interval of < or = 75 ms indicated a high mPCWP (mPCWP > or = 18 mm Hg) with high sensitivity (96%) and specificity (88%). The derived equation was tested in a prospective group of 32 additional patients (aged 43-75 years). A significant correlation was observed between the predicted and measured mPCWP (r = 0.91, p <0.0001). Thus, the PCWP can be estimated by using the D-E interval derived from M-mode mitral echograms in patients in the coronary care unit and in patients with chronic heart disease.

Increased Serum Triglyceride Clearance and Elevated High-Density Lipoprotein 2 and 3 Cholesterol During Treatment of Primary Hypertriglyceridemia with Bezafibrate

BACKGROUND Hypertriglyceridemia accompanied by low levels of high-density lipoprotein cholesterol (HDL-C) is a risk factor for coronary artery disease. High-density lipoprotein 2 (HDL2) and 3 (HDL3) are believed to suppress the progress of atherosclerosis through reverse cholesterol transport. As a result, peripheral tissues can be protected against excessive accumulation of cholesterol. Although bezafibrate is known to accelerate the increase of HDL-C, results are not standardized regarding increases of HDL3 and HDL2 subfractions. OBJECTIVE This study assessed the effects of bezafibrate on serum triglyceride (TG) fractional clearance rate (K2) and HDL2 and HDL3 cholesterol (HDL2-C and HDL3-C, respectively) levels in patients with primary hypertriglyceridemia (serum TG ≥150 mg/dL). METHODS Outpatients with primary hypertriglyceridemia were enrolled in this 8-week study conducted at the Third Department of Internal Medicine, Nagoya City University Hospital (Nagoya, Japan). Oral bezafibrate was administered at a dose of 400 mg/d (200-mg tablet BID, morning and evening) for 8 weeks. After 8 weeks, serum levels of total cholesterol (TC), TG, HDL-C, HDL2-C, and HDL3-C were measured. A fat emulsion tolerance test to assess K2 and measurements of plasma lipoprotein lipase (LPL) mass, LPL activity, and hepatic triglyceride lipase (HTGL) activity in postheparin plasma were performed before bezafibrate administration and after the course of treatment. RESULTS Sixteen patients (10 men, 6 women; mean [SD] age, 54 [12] years [range, 30-69 years]; mean [SD] body mass index, 23 [2] kg/m(2)) entered the study. The following findings were observed in male and female patients after 8 weeks of treatment. A statistically significant reduction was observed in mean serum TG level (P<0.01). Significant increases were seen in HDL-C, HDL2-C, and HDL3-C (all P<0.01), K2 (P<0.01), and in plasma LPL mass (P<0.01) and LPL activity (P<0.05). TC level and HTGL activity did not change significantly. No adverse effects related to the use of bezafibrate were documented. CONCLUSIONS In this study, bezafibrate treatment resulted in significant decreases in serum TG level and significant increases in HDL2-C and HDL3-C levels and plasma LPL mass and activity. We hypothesize that bezafibrate may increase HDL3-C by promoting TG-rich lipoprotein catabolism and may increase HDL2-C by promoting the conversion of HDL3 to HDL2.