[Progression of the left ventricular hypertrophy].
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Biomedical subjects
Publications and source records attributed to N Doba.
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A 47 year old Japanese male with exertional shortness of breath, cardiac murmur and ECG abnormalities was examined with invasive and non-invasive cardiology techniques that disclosed hypertrophic cardiomyopathy, and the anomalous origin of the left coronary artery from the right sinus of Valsalva. Although both situations have been known to cause sudden death especially under a state of strenuous physical stress, his exercise thallium scintigraphy performed with the symptom limited maximal test did not uncover any significant myocardial ischemia or exercise induced malignant arrhythmias. This is a very rare association of two distinctly identified clinical situations highly indicative of a likelihood of sudden cardiac death. Therefore, careful observation is needed.
This is a clinical report of a rare case of Charcot-Marie-Tooth disease associated with dilated cardiomyopathy. A seventy-seven-year-old Japanese male first visited our outpatient clinic with a ten-year history of muscular weakness in his bilateral lower extremities and gait disturbance characterized by classical features of peroneal muscular atrophy and inverted champagne bottle legs. Biopsy findings of the m. quadriceps femoris and the n. gastrocnemius revealed clustered atrophy of myofibrils and segmental demyelinization mingled with remyelinization. Because of his other problem of dilated cardiomyopathy, he had been treated with salt restriction, digitalis, diuretics and vasodilators, until his third hospitalization, when he developed terminal stage of severe congestive heart failure. Despite our intensive cardiac care, the patient died because of profound pump failure. Autopsy findings disclosed a remarkably dilated left ventricular chamber and an increased total heart weight of 600 grams. Grossly, the cross sectional view of the left ventricle revealed diffuse, but not homogenous fibrosis that was most prominent in the posterior wall. On light microscopic examination, the left ventricular myocardium revealed diffusely scattered muscular degeneration interlaced with fibrosis. Although large epicardial coronary arteries revealed only mild intimal atheromatous thickening, most of the small intramuscular coronary arteries were free from atherosclerosis. Neither diabetic nor amyloid lesions could be detected. It has been well known that cardiomyopathy is often associated with various forms of muscular dystrophy and Friedreich's ataxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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To clarify the central effects of physical training on patients with coronary heart disease, 81 subjects were selected for the present study. Evaluations of the oxygen transport system function were performed according to the definition proposed by Bruce and others in terms of FAI (functional aerobic impairment), LVI (left ventricular impairment) or MRI (myocardial reserve impairment), CRI (chronotropic reserve impairment) and PCI (peripheral circulatory impairment). Remarkable improvement in left ventricular impairment was found in those patients with single vessel disease or those who experienced disappearance of chest pain after the completion of the program. In another series of study on myocardial perfusion performed on 11 patients with coronary heart disease, improvement in ischemia was also demonstrated in 7 of 8 patients who revealed redistribution pattern in 201TL exercise stress images specifying myocardial ischemia. In conclusion, exercise training could induce improvements not only the left ventricular functions characterized by increased maximal pressure rate product and maximal heart rate, but also in myocardial ischemia. Further studies are needed to specify its effects, since natural progression or regression of the disease process itself may influence the results.
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Determination of the blood pressure (BP) level in patients with mild hypertension (MHT) is quite difficult, since ulcerations of BP are tremendously exaggerated in the doctor's office. It has been well known that casual BP is less reliable to estimate LVH than BPs obtained at home or work-site. Although 24 hour ambulatory BP monitoring (ABPM) has been widely accepted to overcome this problems, it is still controversial whether this method is applicable to all hypertensive subjects with special regards to its cost and effect. Therefore, our study has dealt mainly with the development of more convenient and less expensive method to get reasonable BPs. Twenty two nonmedicated patients with MHT were selected for the study. After taking casual BP in the office, the resting 20 minute BP measurements at every 2 minute interval were performed with Dynamap 950. Ten BP values thus obtained were divided into two categorical phases; early and late. The mean systolic and diastolic pressures (Ps & Pd) in the early phase were significantly higher than those in the late phase. Beside mean Ps and Pd obtained from 24 hour ABPM, 4 categorical phases based on the time of a day were defined; morning (from awaking to noon), afternoon (from noon to 6 pm), evening (from 6 pm to bed time) and night (during sleeping). Mutual correlation coefficients of these categorical BPs were calculated and compared to identify reasonably high significant correlations. The results revealed the highest BP at the office and the lowest one during sleeping. The office BPs closely resembled to the ones during afternoon period.(ABSTRACT TRUNCATED AT 250 WORDS)
Although extracardiac sounds secondary to cardiac pacing have been well known, the murmurs originating in the heart after permanent pacemaker implantation and then disappearance after exchanging a temporary to permanent lead have rarely been reported. In this paper, two patients revealing a musical systolic murmur after placement of a transvenous endocardial pacemaker in the absence of any complications were documented. Case 1: A 43-year-old man with episodes of dizziness and brady-tachycardiac atrial fibrillation. Immediately after the implantation of a temporary transvenous right ventricular pacemaker, a high-pitched systolic musical murmur was heard at the lower left sternal border. No murmur was however gullible after a permanent pacemaker implantation in this case. Case 2 was a 83-year-old female with coronary heart disease associated with sick sinus syndrome to whom a permanent transvenous right ventricular pacemaker was inserted. A musical systolic murmur occurring immediately after the procedure was best audible at the apex. Although numerous papers concerning the mechanisms of these cardiac murmurs have been reported without reaching conclusive explanations, our data based on two cases examined with Doppler echocardiography did not support the idea of tricuspid regurgitation as one of causative factors. In the first case, this murmur appeared only a temporary pacing was performed and disappeared after implantation of a permanent pacemaker lead. On the contrary, however, the 2nd case revealed after the implantation of the permanent pacemaker with a relatively rigid bipolar lead. It is concluded that these murmurs might be produced by vibrations caused by the pacing catheters and physical properties could be related the mechanism of this phenomenon.
The oxygen transport system (OTS) function was evaluated with multistage treadmill stress testing on 171 normal control subjects and 80 patients with coronary heart disease (CHD). After Bruce's definition, OTS function was expressed with functional aerobic impairment (FAI), left ventricular impairment (LVI) or myocardial aerobic impairment (MAI), heart rate impairment (HRI) or chronotropic reserve impairment (CRI) and peripheral circulatory impairment (PCI). All subjects were monitored on heart rate, blood pressure, electrocardiogram and endtidal O2 and CO2 before and every one minute during the symptom limited maximal stress testing. Seventy three of 80 coronary patients were subjected to the coronary arteriography and were classified into four groups; 31 with single vessel disease (SVD), 20 with double vessel disease (DVD), 15 with triple vessel disease (TVD) and 7 with A-C bypass surgery. Comparison between normal control subjects and the CHD patients with regard to the relation of age and VO2max derived from the linear regression analysis disclosed the identical age-related decrease in VO2max in both groups. The age corrected VO2max in the CHD patients, however, was 2.2 METS less than that of normal control subjects. Therefore, the level of VO2max in CHD patients was determined not only by disease, but also by ageing process itself. Comparisons among three CHD groups with regard to FAI, LVI, HRI and PCI clearly demonstrated different functional impairments paralleling to the severity of the disease process. On the other hand, the patients with A-C bypass surgery revealed almost identical functional impairment to the patients with SVD. In conclusion, these simple and noninvasive evaluations of the oxygen transport system could give us valuable informations reasonably differentiating the clinical status of the patients with CHD.
To investigate the predictive value of exercise tests and diastolic function measurements for the progression of left ventricular hypertrophy, symptom-limited treadmill stress testing and echocardiography were performed before and after a follow-up period of 3.5 years in 47 mild hypertensive men aged 42 +/- 2 years. The men were classified into three groups by the progression of the left ventricular mass index (%LVMI) during the observation, i.e. (LVMI after follow-up) - (LVMI before follow-up)/(LVMI before follow-up). The high-progression group (n = 13) had a %LVMI exceeding mean +/- 2/3s.d. of all subjects; the low-progression group (n = 21) had a %LVMI within mean +/- 2/3s.d. and the non-progression group (n = 13) had a %LVMI less than mean -2/3s.d. At the beginning of the observation, age, blood pressure at rest, LVMI, ejection fraction, mean velocity of circumferential fibre shortening, peak shortening rate and systolic time intervals (ET/PEP, ratio of ejection time to pre-ejection period) were similar among the three groups. However, the high-progression group showed a higher systolic pressure at peak exercise, a lower peak filling rate and a longer time to peak filling rate (TPFR) as corrected by the R-R interval of the ECG. These data suggest that systolic pressure at peak exercise and echocardiographically assessed diastolic function are useful in predicting the progression of cardiac involvement in mild hypertension.
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Changes in the fractional distribution of cardiac output (FF), organ blood flow, and regional vascular resistance were measured by the isotope dilution technique of Sapirstein using 86Rb as indicator in unanesthetized rats during acute arterial hypertension produced by bilateral lesions of the nucleus tractus solitarii (NTS). After NTS lesions, the FF was significantly reduced in skin, muscle, and colon, increased in ventricular myocardium, spleen, and adrenal glands, and was unchanged elsewhere. Because of a marked reduction in cardiac output (CO) during hypertension, the absolute organ blood flow (FF X CO) was reduced in lesioned rats to 30-40% of control in skin, muscle, and colon and between 60% and 75% of control in most of the remainder of the gastrointestinal tract and renal cortex; it was unchanged in myocardium and endocrine glands. Resistance was substantially increased (4- to 6-fold) in skin, muscle and colon but was only moderately increased (1.5- to 2.5-fold) in the remaining organs. The results indicate that, while NTS lesions will increase resistance in most vascular beds, the response is unequally distributed, influencing skin, muscle, and colon disproportionately to other tissues. Because of an interaction between a reduction in CO and little autoregulation, blood flow is reduced primarily in skin, muscle, and colon. The pattern of redistribution of CO was consistent with the interpretation that NTS hypertension results from interrupting baroreceptor reflexes centrally. The pattern of redistribution of blood flow in rats with NTS lesions differs from that produced by deoxycorticosterone acetate-salt and renal ischemia.
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A study was performed on adult cats to investigate synaptic structures of nerve terminals in the commissural portion of the nucleus of the tractus solitarius (NTS); a site where the cardiovascular afferent fibers terminate and where a dense plexus of adrenergic element also resides. Synaptic contacts observed in the commissural portion were predominantly axo-dendritic but a smaller number of axo-somatic synapses were also recognized. A third type of junction, axo-axonic, appears to be unique to the commissural portion of the nucleus, since no axo-axonic contacts were encountered in the medial and ventrolateral portions of the NTS. By labeling with the 'false' neurotransmitter 5-hydroxydopamine (5-OHDA), three types of axo-axonic contacts with different presynaptic components could be identified; namely, axon varicosities with small clear spherical vesicles, axon varicosities containing flat synaptic vesicles and others with small cord vesicles labeled with 5-OHDA. Postsynaptic components were always axon varicosities with clear spherical vesicles. After surgical denervation of the IXth and Xth cranial nerves, no degenerated axon varicosities were observed in the presynaptic side in the axo-axonic contact. The present study clearly demonstrates that the commissural portion of the NTS contains axo-axonic synapses and some of the adrenergic axons in this area provide the presynaptic components for this type of synapse. Possible roles of adrenergic nerves to presynaptic regulation of baroreceptor reflexes are discussed.