Keiji Iida

Cardiac determinants of regression of left ventricular hypertrophy in essential hypertension with antihypertensive treatment

To study the cardiac determinants of regression of left ventricular hypertrophy in hypertension, left ventricular mass, fractional shortening and end-systolic wall stress were measured echocardiographically in 36 patients with essential hypertension and left ventricular hypertrophy. The patients were classified into two groups. Group I consisted of 15 patients with subnormal end-systolic wall stress, and Group II consisted of 21 patients with normal end-systolic wall stress. There were no significant differences between groups in systolic or diastolic blood pressure. After treatment for 4.4 +/- 1.7 years, echocardiographic studies were repeated. There were no significant differences between groups in the duration of the follow-up period and the kinds of antihypertensive drugs. After treatment, blood pressure decreased significantly in both groups (p less than 0.001 for both), with no significant difference between groups. Left ventricular mass increased significantly in Group I (from 331 +/- 7 to 363 +/- 24 g, mean +/- SEM, p less than 0.05), whereas it decreased significantly in Group II (from 318 +/- 16 to 268 +/- 17 g, p less than 0.001). Myocardial contractility (the relation between end-systolic wall stress and fractional shortening) remained almost the same as before treatment. In conclusion, in patients with hypertensive ventricular hypertrophy with subnormal end-systolic wall stress (inappropriate hypertrophy, probably induced by a neurohumoral factor), a decrease in blood pressure with antihypertensive treatment does not lead to regression of left ventricular hypertrophy, but rather to an increase in left ventricular mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Response to isoproterenol as a prognostic indicator of evolution from hypertrophic cardiomyopathy to a phase resembling dilated cardiomyopathy

OBJECTIVES We sought to assess whether isoproterenol stress echocardiography could detect in advance in which patients hypertrophic cardiomyopathy would progress to a phase resembling dilated cardiomyopathy. BACKGROUND In a few patients, hypertrophic cardiomyopathy has been reported to progress to a phase characterized by systolic dysfunction and left ventricular dilation, resembling dilated cardiomyopathy. METHODS Echocardiograms were recorded before and immediately after intravenous infusion of isoproterenol (0.02 microgram/kg body weight per min) for 5 min in 18 patients with typical hypertrophic cardiomyopathy (i.e., hypertrophied, hyperdynamic and nondilated) to determine the difference in fractional shortening. The patients were categorized into those with a good response (difference in fractional shortening > 7%, 14 patients) and those with a poor response (difference < or = 7%, 4 patients). Changes in left ventricular end-diastolic diameter and fractional shortening were evaluated by using serial echocardiography over an average follow-up period of 5.4 years. RESULTS In the good response group, neither end-diastolic diameter nor fractional shortening changed significantly during the follow-up period. In the poor response group, end-diastolic diameter significantly increased from a mean +/- SD of 41 +/- 5 to 53 +/- 5 mm (p < 0.05), and fractional shortening significantly decreased from 40 +/- 12% to 29 +/- 10% (p < 0.05). All patients in the poor response group showed a substantial decrease (> or = 5%) in fractional shortening and an increase (> or = 5 mm) in end-diastolic diameter. One patient developed congestive heart failure due to systolic dysfunction during the observation period. CONCLUSIONS The present study confirmed that impaired responses to isoproterenol infusion are related to future deterioration of left ventricular performance in patients with typical hypertrophic cardiomyopathy.

Enhanced washout of 99mTc-tetrofosmin in hypertrophic cardiomyopathy: quantitative comparisons with regional 123I-BMIPP uptake and wall thickness determined by MRI

The diagnostic value of technetium-99m tetrofosmin (TF) washout in hypertrophic cardiomyopathy (HCM) was examined by investigating its relation to the metabolic abnormality depicted by iodine-123 β-methyl-p-iodophenylpentadecanoic acid (BMIPP) uptake and the left ventricular (LV) myocardial wall thickness as measured by magnetic resonance imaging (MRI). TF washout was evaluated in 31 patients with HCM and 23 normal control subjects using 30-min (early) and 3-h (delayed) TF single-photon emission tomography images. The LV myocardial wall was divided into 19 segments and the percentage TF washout, regional BMIPP uptake and LV wall thickness were measured in each segment. Mean TF washout in the patients with HCM was significantly faster than that in normal control subjects (23.7±5.7 vs 13.4±4.1, P<0.0001). In the patients with HCM, TF washout showed an excellent correlation with MRI wall thickness (r=0.82, P<0.0001) and a good inverse correlation with regional BMIPP uptake (r=−0.72, P<0.0001). In addition, a good linear correlation was observed between TF uptake and MRI wall thickness in the 19 regional segments. In conclusion, the degree of TF washout corresponds well with the severity of myocardial wall thickness and the degree of metabolic abnormality in patients with HCM. These results suggest that enhanced TF washout might provide additional clinical information regarding metabolic alterations in HCM.

Mechanisms of stress-induced ST elevation and negative T-wave normalization studied by serial cardiokymogram in patients with a previous myocardial infarction

Seventeen patients with a previous myocardial infarction were studied during pacing to characterize the clinical correlates of ST elevation, to analyze the relation between ST elevation and negative T-wave normalization and to investigate the mechanism of these electrocardiographic changes. Myocardial ischemia was evaluated by measurement of blood lactate, and wall motion was analyzed using cardiokymographs concurrently and serially. Results show that ST elevation and negative T-wave normalization were most marked in leads containing abnormal Q waves, that ST elevation greater than or equal to 1 mm during pacing was associated with a significant increase in left ventricular end-diastolic pressure and deterioration of left ventricular wall motion and that the magnitude of ST elevation and negative T-wave normalization was significantly correlated, but the latter appeared earlier and more markedly. In addition, there was no significant correlation between the extent of either ST elevation or negative T-wave normalization and myocardial lactate production. Thus, ST elevation and negative T-wave normalization are caused by abnormal left ventricular wall motion rather than myocardial ischemia. Negative T-wave normalization is a more sensitive marker of abnormal wall motion than ST elevation in patients with a previous myocardial infarction.

Quantitative evaluation of myocardial function by a volume-normalized map generated from relative blood flow.

Our study aimed to quantitatively evaluate blood flow in the left ventricle (LV) of apical hypertrophic cardiomyopathy (APH) by combining wall thickness obtained from cardiac magnetic resonance imaging (MRI) and myocardial perfusion from single-photon emission computed tomography (SPECT). In this study, we considered paired MRI and myocardial perfusion SPECT from ten patients with APH and ten normals. Myocardial walls were detected using a level set method, and blood flow per unit myocardial volume was calculated using 3D surface-based registration between the MRI and SPECT images. We defined relative blood flow based on the maximum in the whole myocardial region. Accuracies of wall detection and registration were around 2.50 mm and 2.95 mm, respectively. We finally created a bulls-eye map to evaluate wall thickness, blood flow (cardiac perfusion) and blood flow per unit myocardial volume. In patients with APH, their wall thicknesses were over 10 mm. Decreased blood flow per unit myocardial volume was detected in the cardiac apex by calculation using wall thickness from MRI and blood flow from SPECT. The relative unit blood flow of the APH group was 1/7 times that of the normals in the apex. This normalization by myocardial volume distinguishes cases of APH whose SPECT images resemble the distributions of normal cases.

Addition of spironolactone to an angiotensin-converting enzyme inhibitor decreases lung congestion and edema in Dahl hypertensive rats

We investigated the effect of adding spironolactone to treatment with an angiotensin-converting enzyme (ACE) inhibitor, imidapril, in Dahl salt-sensitive (DS) hypertensive heart failure rats with preserved systolic function. Male DS rats were fed laboratory chow containing 8% NaCl from 7 weeks of age. Rats were divided into four groups and treated for 9 weeks with vehicle alone (water; n = 23), the ACE inhibitor imidapril (1 mg kg−1 day−1; n = 16), spironolactone (2 mg kg−1 day−1; n = 15), or a combination of imidapril and spironolactone at the doses above (n = 16). The left ventricular weight to body weight (BW) ratio was significantly lower in the imidapril group (3.28 ± 0.30 mg g−1) and the combination group (3.34 ± 0.38 mg g−1) than in the vehicle group (3.71 ± 0.46 mg g−1). Adding spironolactone to imidapril inhibited an increase in the ratio of lung weight to BW (4.38 ± 0.50 mg g−1) related to high salt intake, while monotherapy (imidapril group, 4.61 ± 0.90 mg g−1; spironolactone group, 5.40 ± 2.50) did not significantly change the ratio from that seen with vehicle treatment (6.32 ± 3.62 mg g−1). All active treatments (imidapril, 0.66% ± 0.67%; spironolactone, 0.51% ± 0.55%; both together, 0.31% ± 0.26%) inhibited a salt-intake related increase in the percentage area representing fibrous tissue compared with vehicle treatment alone (1.81% ± 1.51%). These findings suggest that adding spironolactone to an ACE inhibitor is more effective in improving pulmonary congestion and edema in hypertensive heart failure with preserved systolic function than an ACE inhibitor alone.

Diffuse and marked breast uptake of both123I-BMIPP and99mTc-TF by myocardial scintigraphy

Unexpected breast uptake was observed in a 32-year-old woman referred for evaluation of hypertrophic cardiomyopathy. Diffuse and marked bilateral breast uptake of123I-BMIPP and99mTc-TF was shown by both planar and SPECT imaging during the first study, and the uptake of both radionuclides had decreased significantly eleven months later. At the time of the first radionuclide examination, she was occasionally breast feeding her 2-year-old child and had small amounts of milk production. At the follow up examination, the frequency of breast feeding was significantly reduced and she produced only small amounts of milk. Therefore, the uptake of123I-BMIPP and99mTc-TF may have been caused by lactation.

Daily variations of ECG and left ventricular parameters at exercise in patients with anginal attacks but normal coronary arteriograms

In 21 patients with typical exercise-induced anginal pain but normal coronary arteriograms (group N) and in 14 patients with angiographically proved coronary stenosis (group C), symptom-limited ergometer exercise ECG and radionuclide angiocardiography were performed twice on two different days. Exercise-induced ST changes showed larger variations between the two exercise tests in group N than in group C ([delta ST1-delta ST2]: 0.07 +/- 0.06 mV in group N, 0.03 +/- 0.03 mV in group C, p less than 0.05). Rate pressure product and left ventricular ejection fraction at exercise also showed larger variations between the two tests in group N than in group C (p less than 0.001, p less than 0.05, respectively). However, substantial overlaps existed in some cases in the two groups. In conclusion, some of the patients with exercise-induced anginal pain but normal coronary arteriograms may have a variable threshold of exertional chest pain probably caused by variation in coronary vascular tone, and the other patients may have a fixed threshold of chest pain caused by other mechanisms.