Hemodynamic response to dietary sodium loading in essential hypertension studied with Doppler echocardiography.

The cardiac response to dietary salt loading was assessed by Doppler echocardiography during various sodium intakes (52-345 mEg per day) in 30 patients with essential hypertension. The Mitral flow velocity integral in the rapid filling phase (IntR) and the atrial contraction phase (IntA) was measured from the transmitral flow pattern, and the sum of IntR and IntA (IntR + IntA), the ratio of IntA to IntR (IntA/IntR), cardiac output (CO) and total peripheral resistance (TPR) were calculated. With salt loading, the mitral flow pattern remained almost unchanged in the nonsalt-sensitive (NSS) patients. Fourteen of the 19 salt-sensitive (SS) patients showed significant increases in IntR + IntA and CO with salt loading (IntR + IntA, from 13.9 +/- 2.8 to 17.9 +/- 3.6 cm, p less than 0.01; CO, from 6021 +/- 2130 to 8305 +/- 1699 ml/min, p less than 0.01), and were termed "salt-sensitive CO-dependent" (SS [COdep]), suggesting that the apparent pressor response to sodium loading was mediated by an increased CO. In the remaining five SS patients termed "salt-sensitive CO-independent" (SS [COindep]), IntA/IntR increased significantly with sodium repletion (from 0.66 +/- 0.23 to 0.90 +/- 0.31, p less than 0.01), without a significant change in IntR + IntA. Increments in IntA/IntR observed in the SS [COindep] patients were considered to be due to an elevation of total peripheral resistance (TPR), since changes in IntA/IntR were significantly correlated with those in TPR in all subjects (r = 0.617, p less than 0.01).

Malignant lymphoma of the lung: report of an autopsy case and review of literature.

A 74-year-old man complained of a cough and left chest pain. Chest X-ray showed marked pleural effusion and a large mass in the left lower lobe, and air bronchograms within the mass were observed by tomography and computed tomography (CT). About 3 months later, the patient died of left atelectasis and pneumonia. Autopsy revealed a localized tumor in the lower lobe of the left lung. Histologically, proliferation of lymphoma cells was noted. Immunoglobulin staining showed B cell-type monoclonality. No metastasis was evident except for a very small nodular area in the left renal cortex.

[Effects of verapamil and disopyramide phosphate on the termination, reinduction and long-term prevention of paroxysmal supraventricular tachycardia].

The efficacy of verapamil and disopyramide phosphate for the termination and prevention of paroxysmal supraventricular tachycardia (PSVT) were studied electrophysiologically in 32 patients with inducible sustained PSVT (17 patients received verapamil, 15 patients received disopyramide). Twelve patients had atrioventricular nodal tachycardia, 7 had concealed and 13 had overt Wolff-Parkinson-White syndrome. Intravenous verapamil (0.15 mg/kg) terminated the sustained PSVT in 15 of the 17 patients (88%) by production of AV block in 13 patients, VA block in one, and a ventricular premature beat in one. PSVT could not be induced in any of these 15 patients after they had received verapamil. In the remaining 2 patients, PSVT could not be terminated by the use of verapamil, but the cycle lengths of PSVT were lengthened. Long-term oral dosages of verapamil of 120-240 mg/day were administered in 13 of the 17 patients. All patients except two, whose PSVT was unable to be effected by intravenous verapamil, were well controlled: PSVT disappeared in 7 patients and decreased in 4. Intravenous disopyramide (1.5 mg/kg) terminated induced PSVT in 10 of the 15 patients (67%) by production of VA block. Although PSVT could not be reinitiated in 5 of these 10 patients, non-sustained PSVT was induced in 2 and sustained PSVT was induced in 3 after having received disopyramide. PSVT was induced in all of the 5 patients who failed to respond to disopyramide. The cycle lengths of PSVT after administration of disopyramide remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

[Left ventricular diastolic reserve during acute pressure loading in hypertrophic cardiomyopathy and dilated cardiomyopathy].

To evaluate left ventricular diastolic reserve during acute pressure loading, changes in mitral flow velocity patterns before and after the elevation of blood pressure were analyzed by pulsed Doppler echocardiography in 11 cases of hypertrophic cardiomyopathy (HCM), nine cases of dilated cardiomyopathy (DCM), and 11 control subjects. Systolic blood pressure was elevated 25% above basal values by methoxamine infusion (0.01 mg/kg/min). Before and after methoxamine, left ventricular dimension and mitral flow velocity pattern were obtained by M-mode and pulsed Doppler echocardiography, respectively. The peak velocity in the rapid filling and atrial contraction phases and time-velocity integrals were measured from the flow pattern. After methoxamine, left ventricular diastolic dimension was significantly increased in all groups, from 43.8 +/- 4.7 mm to 47.4 +/- 4.9 mm in the control subjects, from 43.7 +/- 6.3 mm to 47.2 +/- 6.0 mm in HCM, and from 57.9 +/- 6.4 mm to 60.6 +/- 5.9 mm in DCM. Left ventricular systolic dimension was significantly increased from 48.6 +/- 8.4 mm to 52.8 +/- 8.3 mm in DCM, but not in the control subjects or HCM. The peak velocity in the rapid filling phase was significantly increased from 60 +/- 16 cm/sec to 69 +/- 14 cm/sec in the control subjects and tended to be increased from 44 +/- 13 cm/sec to 52 +/- 12 cm/sec in HCM. The extent of this increase tended to be less in HCM. However, the peak velocity in the rapid filling phase tended to decrease in DCM. There were no consistent trends of changes in the peak velocity in the atrial contraction phase in any groups. The mitral velocity integral increased from 502 Hz-sec to 621 Hz-sec in the controls and from 525 Hz-sec to 613 Hz-sec in HCM, but it did not increase in DCM. These findings suggest that there is impaired diastolic reserve during acute pressure loading in HCM and DCM and that the diastolic disturbance might be reflected in the early diastolic phase, rather than in the late diastolic phase.

Premature opening of the pulmonary valve in endomyocardial fibrosis.

Two-dimensional and Doppler echocardiographic findings in a 67-year-old man with endomyocardial fibrosis (EMF) are described. The two-dimensional echocardiogram showed typical features of EMF, right ventricular endomyocardial calcification, a thickened right ventricular wall, obliteration of the apex of the right ventricle and marked dilatation of the right atrium. In addition, premature opening of the pulmonary valve was observed during late diastole. The Doppler echocardiogram revealed forward flow from the right ventricle to the pulmonary artery, indicating the conduit state of the right ventricle. These findings were supported by cardiac catheterization and autopsy. Thus, two-dimensional and Doppler echocardiography are useful not only in making the diagnosis, but also in understanding the hemodynamic condition in EMF.

[Echo and Doppler cardiographic findings of isolated quadricuspid aortic valve: a case report and a review of the literature].

The two-dimensional and pulsed Doppler echocardiographic features of a case of isolated quadricuspid aortic valve with aortic regurgitation are described. A 62-year-old woman was hospitalized for exertional palpitation and dyspnea. Her physical examination showed the typical findings of aortic regurgitation. Two-dimensional echocardiograms revealed the aortic valve to have four cusps of nearly equal size. The accessory cusp was situated between the right and left coronary cusps. By pulsed Doppler echocardiography, holodiastolic turbulent flow signals were observed in the left ventricle, and the aortic flow pattern showed holodiastolic reverse flow, indicating severe aortic regurgitation. These findings were confirmed by aortography and by surgery. The coronary arteries and pulmonary valve were normal. We attempted a classification of the anatomical variations of the previously reported 34 cases of isolated quadricuspid aortic valves, including our own. They were classified as one smaller (67%), four equal (18%), three smaller (6%), four unequal (6%) and two smaller (3%) types. Twenty of the 34 patients had aortic regurgitation. Bacterial endocarditis and congestive heart failure were the main causes of death.

[Analysis of mitral inflow velocity pattern in relation to left ventricular end-diastolic pressure].

The relationship between mitral inflow velocity patterns and left ventricular end-diastolic pressure (LVEDP) was evaluated using pulsed Doppler echocardiography in 34 cases of heart disease, without significant valvular regurgitation. Flow patterns in 19 of the 34 cases were also examined before and after the elevation of LVEDP by methoxamine infusion, 0.01 mg/kg/min. The ratio of the peak velocities in the atrial contraction phase to that in the rapid filling phase (A/R) and the ratio of mean acceleration rates to peak velocities in the rapid filling phase (ACR/R) were determined from the mitral flow patterns obtained by the apical approach. 1. ACR/R correlated significantly with LVEDP (r = 0.49), but A/R did not. LVEDP in six cases with normal A/R (0.5 to 1.0) was 8.3 +/- 2.9 mmHg (mean +/- SD). Among 19 cases with A/R of 1.0 or more and ACR/R less than 13 sec-1, LVEDP showed 10.2 +/- 3.8 mmHg. In eight cases with A/R of 1.0 or more and ACR/R of 13 sec-1 or more, LVEDP was 17.9 +/- 6.2 mmHg. The average value of LVEDP in two cases with A/R less than 0.5 was 18.5 mmHg. 2. When the LVEDP was elevated after methoxamine infusion, A/R within normal range increased in five of six cases and decreased in the remaining case. A/R more than 1.0 decreased in 10 of 11 cases and ACR/R tended to increase with increasing LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)