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PubMed1999

Intracellular sodium accumulation during ischemia as the substrate for reperfusion injury.

To elucidate the role of intracellular Na+ kinetics during ischemia and reperfusion in postischemic contractile dysfunction, intracellular Na+ concentration ([Na+]i) was measured in isolated perfused rat hearts using 23Na nuclear magnetic resonance spectroscopy. The extension of the ischemic period from 9 minutes to 15, 21, and 27 minutes (at 37 degrees C) increased [Na+]i at the end of ischemia from 270.0+/-10.4% of preischemic level (mean+/-SE, n=5) to 348.4+/-12.0% (n=5), 491.0+/-34.0% (n=7), and 505.3+/-12.1% (n=5), respectively, whereas the recovery of developed pressure worsened with the prolongation of the ischemic period (95.1+/-4.2%, 84.3+/-1. 2%, 52.8+/-13.7%, and 16.9+/-6.4% of preischemic level). The kinetics of [Na+]i recovery during reperfusion was analyzed by the fitting of a monoexponential function. When the hearts were reperfused with low-[Ca]o (0.15 mmol/L) solution, the time constants of the recovery (tau) after 15-minute (8.07+/-0.85 minutes, n=5) and 21-minute ischemia (6.44+/-0.90, n=5) were significantly extended, with better functional recovery (98.5+/-1.4% for 15-minute [P<0.05]; 98.0+/-1.0% for 21-minute [P<0.05]) compared with standard reperfusion ([Ca]o=2.0 mmol/L, tau=3.58+/-0.28 minutes for 15-minute [P<0.0001]; tau=3.02+/-0.20 for 21-minute [P<0.0001]). A selective inhibitor of Na+/Ca2+ exchanger also decelerated the [Na+]i recovery, which suggests that the recovery reflects the Na+/Ca2+ exchange activity. In contrast, high-[Ca]o reperfusion (5 mmol/L) accelerated the [Na+]i recovery after 9-minute ischemia (tau=2.48+/-0.11 minute, n=5 [P<0.0001]) and 15-minute ischemia (tau=2.10+/-0.07, n=6 [P<0. 05]), but functional recovery deteriorated only in the hearts with 15-minute ischemia (29.8+/-9.4% [P<0.05]). [Na+]i recovery after 27-minute ischemia was incomplete and decelerated by low-[Ca]o reperfusion, with limited improvement of functional recovery (42. 5+/-7.9%, n=5 [P<0.05]). These results indicate that intracellular Na+ accumulation during ischemia is the substrate for reperfusion injury and that the [Na+]i kinetics during reperfusion, which is coupled with Ca2+ influx, also determines the degree of injury.

Animals↗
PubMedDate not supplied

Cardiac cycle-dependent alternating flow in vertebral arteries with subclavian artery stenoses.

Continuous-wave Doppler sonography is a reliable method for detecting severe subclavian stenosis and occlusion as well as subclavian steal. Intermediate stages leading to subclavian steal can also be detected. These are characterized by a cardiac-phase-dependent alternating flow direction in the vertebral artery. Some cases of proximal subclavian or proximal vertebral artery stenosis produce a systolic deceleration of flow in the vertebral artery. Stenosis and occlusion of the subclavian artery as well as stenosis of the subclavian and vertebral arteries can be distinguished. The pulse curve changes described can be reversed by a vascular by-pass. Alternating flow direction or systolic deceleration of flow in the radial artery could also be observed or induced in a iatrogenic model using Cimino's a-v fistula in the arm in patients on dialysis. The results in beginning subclavian steal situations can be applied in principle to other collateral circulations, and in particular to the hemodynamics in the region of watersheds.

Arterial Occlusive Diseases↗
PubMedDate not supplied

Pulmonary venous flows reflect changes in left atrial hemodynamics during mitral balloon valvotomy.

Patients with mitral stenosis have usually blunted pulmonary venous (PV) flow, because of decreased mitral valve area and diastolic dysfunction. The authors compared changes in Doppler PV velocities by using transesophageal echocardiography (TEE) against hemodynamics parameters before and after mitral balloon valvotomy to observe relevance of PV velocities and endsystolic left atrial (LA) pressure-volume relationship. In 25 patients (aged 35 +/- 17 years) with mitral stenosis in sinus rhythm, changes in LA pressure and volumes were compared with PV velocities before and after valvotomy. Mitral valve area, mitral gradients, and deceleration time were obtained. Mitral valve area and mitral gradients changed from 1 +/- 0.2 cm2 and 14.6 +/- 5.4 mmHg to 1.9 +/- 0.3 cm2 and 6.3 +/- 1.7 mmHg, respectively (p<0.001). AR peak reverse flow velocity and AR duration decreased from 29 +/- 13 cm/s and 110 =/- 30 msec to 19 +/- 6 cm/s and 80 +/- 29 msec respectively (p<0.001). Transmitral Doppler E wave deceleration time decreased from 327 +/- 85 to 209 +/- 61 s and cardiac output increased from 4.2 +/- 1.0 to 5.2 +/- 1.1 L/minute (p<0.001). The changes in LA pressure were correlated with changes in S/D (r=0.57, p<0.05). The changes in endsystolic LA pressure-volume relationship were also correlated with changes in S/D (r=0.52, p<0.05). Endsystolic LA pressure-volume relationship decreased after mitral balloon valvotomy, as a result of a large decrease in pressure. PV systolic/diastolic (S/D) waves ratio reflects endsystolic LA pressure-volume relationship and may be used as another indicator of successful valvotomy.

Adult↗
PubMedDate not supplied

Effects of afterload increase on systolic and diastolic functions of the myocardium after myocardial infarction.

The evaluation of noninfarcted zone function after myocardial infarction by the use of noninvasive methods is very important. The authors speculated that phenylephrine, which increases systemic vascular resistance and blood pressure and has no effect on central ischemic and border-zone myocardium but does have an effect on remote myocardium, could be used as a stress agent as information is gathered about the functional capacity of the left ventricle and the status of coronary arteries in patients with recent myocardial infarction. Forty-six patients with recent myocardial infarction (5 women, 41 men; mean age: 53.6 +/-9.3 years) and 15 individuals with normal findings from coronary angiography and ventriculography (9 women and 6 men; mean age: 39.0 +/-11.2 years) were included in the study. The study was performed on the 4th or 5th day of the myocardial infarction. Preejection period/left ventricular ejection time (PEP/LVET), diastolic mitral flow velocity, isovolumic relaxation time (IVRT), and deceleration time (DT), were measured before and after the phenylephrine infusion, with M-mode, pulse wave, and continuous-wave echocardiography. After pressor stress with phenylephrine infusion, all the parameters were measured again. Coronary angiography and ventriculography were performed on all the patients on the 7th to 10th day of the myocardial infarction. All the patients were grouped according to their ejection fraction and the number of involved coronary arteries. The increase in the PEP/LVET ratio in Group 1 (left ventricle ejection fraction [EF] below 40%) and multivessel coronary artery lesion group was significant (p<0.01). PEP/LVET ratio decreased significantly in both Group C (patients with normal-appearing coronary arteries and ventriculographies) and the single-vessel coronary disease group. Although the early diastole flow/atrial systole flow (E/A) ratio increased significantly in the 3 groups, the 0.5 and more increase in E/A ratio had high sensitivity (86%) and specificity (80%) in differentiating the low EF group. The 0.5 and more increase in E/A ratio had 65% sensitivity and 69% specificity in differentiating the multivessel coronary stenosis group. A deceleration time of 130 msec and below in basal conditions had a high sensitivity (86%) and specificity (92%) for detecting the group in which EF was below 40%. After phenylephrine infusion, the shortening of IVRT was significant in Group 1 (p<0.01). Phenylephrine, which has been shown to be an alpha-1 receptor agonist in low doses and effective only on remote myocardial function, may be given with low complication rates in the early postinfarction period. The increase in PEP/LVET ratio, 0.5 and more increase in E/A ratio, and shortening of DT and IVRT after phenylephrine infusion may be indicators of low LV functional capacity and widespread coronary artery disease. This test may suggest performance of early invasive detection of coronary artery disease and early revascularization. This study may also be interesting from a pathophysiological point of view.

Adult↗
PubMed1998

Does the onset of neonatal seizures correlate with the timing of fetal neurologic injury?

The onset of seizures after birth has been considered evidence of an intrapartum asphyxial event. The present study was undertaken to determine whether the timing of neonatal seizures after birth correlated with the timing of a fetal asphyxial event. Thus, singleton term infants diagnosed with hypoxic ischemic encephalopathy and permanent brain injury had a mean birth to seizure onset interval of 9.8 +/- 17.7 (range 1-90) hours. When these infants were categorized according to their fetal heart rate (FHR) patterns, the acute group (normal FHR followed by a sudden prolonged FHR deceleration that continued until delivery) tended to have earlier seizures than infants did within the tachycardia group (normal FHR followed by tachycardia, repetitive decelerations, and diminished variability) and the preadmission group (persistent nonreactive FHR pattern intrapartum). These seizure intervals were as follows: acute, 6.6 +/- 18.0 (range 1-90) hours; tachycardia, 11.1 +/- 17.1 (range 1-61) hours; and preadmission, 11.8 +/- 17.9 (range 1-79) hours (p < 0.05). But the range varied widely and no group was categorically distinct. In conclusion, the onset of neonatal seizures after birth does not, in and of itself, appear to be a reliable indicator of the timing of fetal neurologic injury.

Asphyxia Neonatorum↗
PubMedDate not supplied

An EMG analysis of the shoulder in pitching. A second report.

This is the second report in a series of projects dealing with electromyographic (EMG) analysis of the upper extremity during throwing. Better understanding of the muscle activation patterns could lead to more effective preseason conditioning regimens and rehabilitation programs. Indwelling wire electrodes recorded the output from the biceps, long and lateral heads of the triceps, pectoralis major, latissimus dorsi, serratus anterior, and brachialis for four professional baseball pitchers. These signals were synchronized electronically with high speed film records of a fast ball. The EMG signals were converted from analog to digital records. Results showed that wind-up and early cocking phases showed minimal activity in all muscles, and such firing which occurred was of low intensity. Late cocking, which occurred after the front foot was firmly planted, showed moderate activity in the biceps. Cocking was terminated by the pectoralis major and latissimus dorsi. At this point, the trunk began to rotate forward, while the arm remained elevated and the elbow flexed. Also, the shoulder was moving to maximum external rotation. During the acceleration phase, the biceps was notably quiescent, while the pectoralis major, latissimus dorsi, triceps, and serratus anterior were all active. Muscle action at this time terminated external rotation and elbow flexion; i.e., the muscles fired as decelerators and also initiated the opposite actions for ball acceleration, internal rotation and elbow extension. Follow-through was not only a time of eccentric contraction with muscle activity decelerating the upper extremity complex, it was also an active event with the shoulder moving across the body and the elbow into extension with forearm pronation.

Adult↗
PubMedDate not supplied

Glenoid labrum tears related to the long head of the biceps.

Tears of the glenoid labrum were observed in 73 baseball pitchers and other throwing athletes who underwent arthroscopic examination of the dominant shoulder. Most of the tears were located over the anterosuperior portion of the glenoid labrum near the origin of the tendon of the long head of the biceps muscle into the glenoid. At arthroscopy, the tendon of the long head of the biceps appeared to originate through and be continuous with the superior portion of the glenoid labrum. In many cases it appeared to have pulled the anterosuperior portion of the labrum off the glenoid. This observation was verified at arthroscopy by viewing the origin of the biceps tendon into the glenoid labrum as the muscle was electrically stimulated. With stimulation of the muscle, the tendinous portion became quite taut, particularly near its attachment to the glenoid labrum, and actually lifted the labrum off the glenoid. Three-dimensional high-speed cinematography with computer analysis revealed that the moment acting about the elbow joint to extend the joint through an arc of about 50 degrees was in excess of 600 inch-pounds. The extremely high velocity of elbow extension which is generated must be decelerated through the final 30 degrees of elbow extension. Of the muscles of the arm that provide the large deceleration forces in the follow-through phase of throwing, only the biceps brachii traverses both the elbow joint and the shoulder joint. Additional forces are generated in the biceps tendon in its function as a "shunt" muscle to stabilize the glenohumeral joint during the throwing act.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

The quantitative measurement of normal passive medial and lateral patellar motion limits.

To quantify normal motion, medial and lateral passive patellar motion limits were measured in 67 high school athletes randomly selected from a group of 1340 athletes undergoing preseason physical examinations. Patellar displacement was measured at knee flexion angles of 0 degree and 35 degrees, using both a Patella Pusher (a hand-held force gauge) and a manual technique, and the results were compared. Demographic data and physical examination of the deceleration mechanism (Q angle, vastus medialis obliquus dysplasia, patella alta and baja, and valgus and varus alignment) were correlated with patellar motion limits. With the knee in extension, passive displacement of the patella averaged 9.6 mm medially and 5.4 mm laterally. In flexion, medial displacement averaged 9.4 mm and lateral displacement averaged 10.0 mm. No positive correlations were found between demographic data or deceleration mechanism examination parameters and patellar motion limits, suggesting that motion produced by the displacement force was limited by ligamentous restraints only. The clinical assessment of the passive limits of patellar motion should include examination at knee flexion angles of 0 degree and 35 degrees. The manually produced displacement was found to be more reproducible than displacement by the Patella Pusher (P < 0.05).

Adolescent↗
PubMed2006

Effect of on-line hemodiafiltration with endogenous reinfusion (HFR) on the calcium-phosphorus metabolism: medium-term effects.

AIM: The purpose of the study was to examine the effect of hemodiafiltration with endogenous reinfusion (HFR) compared to hemodialysis (HD) on 28 uremic patients with secondary hyperparathyroidism (2HPT) but positively selected for good and stable control of phosphatemia in order to evaluate the independent effects of dialysis treatments on bone turnover metabolism. METHODS: The study was divided into 3 periods of observation: a) HD for three months; b) HFR for three months; c) HFR for a further 3 months. We analysed the trend of: whole PTH, 1-84 PTH, 7-84 PTH, alkaline phosphatase and its bone isoenzyme, total and ionised calcium, phosphatemia, dose of phosphate binder agents, beta2-microglobulin, CRP. All the variations found were evaluated through mean values +/- SD, t-tests, multivariate analysis. RESULTS: We observed a deceleration in bone turnover characterized by a reduction of the total and bone alkaline phosphatase (IU/mL) from 92.3 +/- 82.8 and 35.8 +/- 49.8 at the end of HD to 63.4 +/- 23.9 and 16.0 +/- 8.7 at the end of HFR, respectively, and 1-84 PTH from 317.5 +/- 264.6 pg/mL at the end of HD to 287.5 +/- 258.9 pg/mL at the end of the 3rd month of HFR. Beta2-microglobulin was reduced from 32.9 +/- 16.1 mg/L at the end of HD to 26.4 +/- 8.1 mg/L already at the end of the first three months of HFR. CRP was reduced from 2.5 +/- 2.6 mg/dL at the beginning of the study to 1.3 +/- 1.7 mg/dL at the end of HFR. There were no differences with regard to: dialytic efficiency, nutritional status, calcemia, phosphatemia (maintained in the K-DOQI range for the entire duration of the study), also thanks to more careful use of phosphate chelating agents. CONCLUSION: We are of the opinion that HFR - essentially thanks to the use of ultrapure endogenous infusate - induces a deceleration in bone turnover due to 2PHT. In addition, phosphate subtraction in HFR is better compared to HD, thanks to the improvement of the anti-inflammatory conditions by removing the cytokines harmful to bone metabolism and excluding a priori the negative effects related to hyperphosphatemia.

Aged↗
PubMed2001

Assembling a clock for all seasons: are there M and E oscillators in the genes?

The hypothesis is advanced that the circadian pacemaker in the mammalian suprachiasmatic nucleus (SCN) is composed at the molecular level of a nonredundant double complex of circadian genes (per1, cry1, and per2, cry2). Each one of these sets would be sufficient for the maintenance of endogenous rhythmicity and thus constitute an oscillator. Each would have slightly different temporal dynamics and light responses. The per1/cry1 oscillator is accelerated by light and decelerated by darkness and thereby tracks dawn when day length changes. The per2 /cry2 oscillator is decelerated by light and accelerated by darkness and thereby tracks dusk. These M (morning) and E (evening) oscillators would give rise to the SCN's neuronal activity in an M and an E component. Suppression of behavioral activity by SCN activity in nocturnal mammals would give rise to adaptive tuning of the endogenous behavioral program to day length. The proposition-which is a specification of Pittendrigh and Daan's E-M oscillator model-yields specific nonintuitive predictions amenable to experimental testing in animals with mutations of circadian genes.

Animals↗
PubMed2005

Evaluating large saccades in patients with brain-stem or cerebellar disorders.

Clinicians conventionally test saccades at the bedside by noting the accuracy, initiation time, and speed of large movements, with the patient's head stationary. Partly for methodological reasons, laboratory analysis of saccades has mainly focused on movements of 20 degrees or less. By measuring the velocity waveform of large saccades, it is possible to examine more closely the way in which brain stem and cerebellum guide the eye to the target. Large saccades made by healthy humans show a positively skewed velocity profile. Slow saccades made by patients with brain-stem disorders show a prolonged plateau of low velocity. Some patients with cerebellar disorders may show increased acceleration and deceleration of saccades. Each of these velocity waveforms can be modeled by changing the parameters that describe medium-lead burst neuron firing. In certain other brain-stem and cerebellar disorders, transient decelerations or premature terminations of saccades occur; such velocity waveforms cannot be modeled solely by changing the parameters that describe burst neuron firing. Instead, it is necessary to postulate dysfunction of the mechanism that normally inhibits pontine omnipause neurons, thereby permitting burst neurons to discharge until the saccade is completed. Analysis of large, abnormal saccades calls for application of novel techniques to identify the beginning and end of the saccadic pulse command.

Adult↗
PubMed1988

Fetal heart rate and transcutaneous monitoring during experimentally induced hypoxia in the fetal dog.

A model of impaired oxygen delivery, using an acute surgical preparation in the fetal dog, is described. Fetal heart rate, transcutaneous pO2 and pCO2, and tissue pH were simultaneously recorded during hypoxic episodes produced by a series of successive occlusions of the maternal abdominal aorta. Corresponding values were also determined in the arterial blood of the fetus. The following pathophysiologic sequence of events was observed: 1) a latency period with no changes; 2) a drop in pO2 which stabilized later at a lower pressure; 3) late fetal heart rate deceleration, the pattern of which was not related to the progressively deteriorating fetal condition; 4) a progressive increase in pCO2; 5) a progressive decrease in pH. Abnormal tissue values consistently preceded and were more adversely affected than corresponding blood values. This experimental model demonstrates first that late decelerations of the fetal heart rate are an early sign of fetal hypoxia and second that a fall in fetal blood pH, beyond that level normally seen during labor, occurs relatively late in this pathophysiologic sequence. Between these two, there are intermediary stages that could be continuously monitored in order to identify worsening fetal condition. Continuous tissue pH and transcutaneous pO2 and pCO2 recording may potentially be of significant clinical value.

Animals↗
PubMed1995

Brain injury without head injury. Some physics of automobile collisions with particular reference to brain injuries occurring without physical head trauma.

The classic kinematic formula, a=(v2-v0(2))/2s, relating deceleration to change of velocity and displacement during the change, is used to determine the acceleration experienced by the occupants of motor vehicles (and their heads) during collisions. The displacement, s, of the occupants in the accident can often be determined from the deformation of the wreckage, thus yielding this critical information about potential for brain injury. Data from 15 accidents are assembled and approximate accelerations computed. At the same time medical and neuropsychological data have been obtained for each of the accident victims. These accidents and the associated victims (except for one special case) have been selected because in no case has the victim suffered a direct head-contact injury. Nevertheless, all suffered neurologic and/or neuropsychological injuries typical of patients with closed head trauma. The paper demonstrates that with decelerations from 30 g to more than 200 g yet without skull impacts, brain damage results.

Journal Article↗
PubMed2003

The neuropsychology of repeated 1- and 3-meter springboard diving among college athletes.

This study examined the neuropsychological effects of repeated springboard diving. It was hypothesized that the impact velocity, which can range from 20 to 30 mph, and accompanying deceleration in the water may lead to concussions and affect the diver's cognitive function. Six varsity National Collegiate Athletic Association Division 1 springboard divers participated in the study. Each diver performed a total of 50 practice dives from either the 1- or 3-m springboard. After each set of 10 dives, the participants were immediately evaluated at poolside using the Symbol Digit Modalities Test, the Stroop Color Word Test, and the Trail Making Test B. Baseline testing revealed, consistent with their athletic specialty, clear neurocognitive strengths among the divers on tests sensitive to proprioception, motor speed, and visual-spatial organization. Results from the serial assessments indicated no detectable neuropsychological deficits among competitive divers compared to baseline testing. Skilled diving at the collegiate level appears to be a safe sport and water appears to present the perfect medium for gradual deceleration. More studies, however, are warranted for 5-, 7.5-, and 10-m platform diving since the impact velocity of the diver from these heights is higher.

Adult↗
PubMed1986

Gonadal regulation of hypothalamic gonadotropin-releasing hormone release in primates.

This review has examined, in primates, the action of sex steroids on the neural timing mechanism that governs the intermittent release of GnRH by the hypothalamus, the so-called GnRH pulse generator. Determinants of hypothalamic GnRH pulse generator frequency have generally been examined indirectly by monitoring moment to moment fluctuations in circulating LH concentrations. Studies using this approach have led to the hypothesis that negative feedback control of LH secretion by the testes is mediated by the action of T, or of one of its metabolites, to retard the frequency of the GnRH pulse generator. P also appears capable of decelerating GnRH pulse frequency during the luteal phase of the menstrual cycle, but the physiological significance of this phenomenon remains to be clarified. To date, a cognate action of E2 on the GnRH pulse generator has not been described. Because of limitations in contemporary technology, the factors underlying amplitude modulation of the GnRH pulse generator are less well understood. In addition to the ability of certain sex steroids to decelerate the frequency of pulsatile GnRH discharge, E2 and P appear capable of facilitating the secretion of this hypothalamic releasing factor. However, the increase in GnRH pulse frequency and/or GnRH pulse amplitude that must underlie these stimulatory actions remains to be fully defined. An inhibitory action of high levels of circulating cortisol on the hypothalamic GnRH pulse generator has also been noted.

Animals↗
PubMed1986

Extracellular calcium is required for copper-amplified prostaglandin E2 stimulation of the release of gonadotropin-releasing hormone from median eminence explants.

Prostaglandin E2 (PGE2) is known to stimulate the release of LHRH from hypothalamic tissue incubated under in vitro conditions. We have previously shown that a short preincubation of explants of the median eminence area with copper(II) [Cu(II)] complexed to histidine (CuHis) markedly amplifies PGE2 stimulation of LHRH release. In this study, we wished to ascertain if Cu-amplified PGE2 stimulation of LHRH release is dependent on influx of extracellular calcium (Ca) and, if so, whether it is the copper and/or PGE2 action that is Ca dependent. Median eminence area explants were incubated for 5 min with 200 microM CuHis, then for 15 min with 10 microM PGE2, and finally for 45 min in buffer (Cu/PGE2). Controls were incubated with CuHis or PGE2. In the presence of Ca (1.8 mM), Cu/PGE2 stimulation of LHRH release reached a peak value within 15 min of exposure to PGE2 (accelerated phase), after which the rate of release declined, with a half-life of about 20 min (decelerated phase). In the absence of Ca, Cu/PGE2 stimulation of LHRH release was inhibited by 70% during the accelerated phase, and it was completely inhibited during the decelerated phase. When incubation was carried out in the presence of Ca and 100 microM verapamil, Cu/PGE2 stimulation of LHRH release was similar to that seen in the absence of extracellular Ca. When Ca was omitted from the incubation medium during the exposure to CuHis but was included during and after the exposure to PGE2, the response to PGE2 was fully restored. In addition, we evaluated the extracellular Ca requirement for stimulation of LHRH release by PGE2 alone (without pretreatment with CuHis) and found that release was inhibited by 65% in the absence of Ca. These results indicate that the process of PGE2 stimulation of LHRH release is partially dependent on extracellular Ca, that the process of Cu-amplified PGE2 stimulation of release is highly dependent on influx of extracellular Ca, and that PGE2 action, but not Cu action, is dependent on Ca influx. Since cAMP has been implicated in Ca2+-dependent secretion in other cells, we propose that Cu amplifies the functional state of a postreceptor component involved in the Ca-cAMP secretory pathway stimulated by PGE2.

Animals↗
PubMed2005

Reversible diastolic dysfunction after long-term exogenous subclinical hyperthyroidism: a randomized, placebo-controlled study.

BACKGROUND: Subclinical hyperthyroidism has been reported to affect systolic and diastolic cardiac function. However, the reversibility of these effects is not well established. OBJECTIVE: Our objective was to investigate the presence and reversibility of cardiac abnormalities in patients with long-term exogenous subclinical hyperthyroidism. DESIGN: We conducted a prospective, single-blinded, placebo-controlled randomized trial of 6 months duration with two parallel groups. SETTING: The study occurred at the Leiden University Medical Center, a tertiary referral center for thyroid carcinoma. PATIENTS: As a model for subclinical hyperthyroidism, 25 patients with a history of differentiated thyroid carcinoma with more than 10 yr of TSH suppressive therapy with L-T4 were studied. INTERVENTIONS: L-T4 dose was replaced by study medication containing L-T4 or placebo. Medication was titrated in a single-blinded fashion to establish continuation of TSH suppression (low-TSH group) or euthyroidism (euthyroid group). MEASUREMENTS: We assessed serum levels of free T4 and TSH and used echo Doppler cardiography including tissue Doppler to establish left ventricular (LV) dimensions and function as well as diastolic function. Baseline echocardiography data were compared with 24 controls. RESULTS: There were no differences in baseline cardiac parameters and TSH levels between the two groups. Although mean LV mass index was increased as compared with 24 controls, only four patients had LV hypertrophy at baseline. This was not improved by restoration of euthyroidism. At baseline, diastolic function was impaired in all patients as indicated by abnormal values for the peak flow of the early filling phase (E, 55.3 +/- 9.5 mm/sec), the ratio of E and the peak flow of the atrial filling phase (E/A ratio, 0.87 +/- 0.13), the early diastolic velocity obtained by tissue Doppler (E', 5.7 +/- 1.3 cm/sec), and the peak atrial filling velocity obtained by tissue Doppler (A', 6.8 +/- 1.4 cm/sec), prolonged E deceleration time (234 +/- 34 msec), and isovolumetric relaxation time (121 +/- 15 msec). After 6 months, significant improvements were observed in the euthyroid group in the E/A ratio (+41%; P < 0.001), E deceleration time (-18%; P = 0.006), isovolumetric relaxation time (-25%; P < 0.001), E' (+31%; P < 0.001), and the E'/A' ratio (+40%; P < 0.001). CONCLUSIONS: We conclude that prolonged subclinical hyperthyroidism is accompanied by diastolic dysfunction that is at least partly reversible after restoration of euthyroidism. Because isolated diastolic dysfunction may be associated with increased mortality, this finding is of clinical significance.

Adult↗
PubMed1991

Enhanced left ventricular diastolic function in hyperthyroidism: noninvasive assessment and response to treatment.

Hyperthyroidism is associated with a marked effect on the cardiovascular system. Despite enhanced resting ventricular systolic performance, thyrotoxicosis has been implicated as a primary cause of cardiomegaly, congestive heart failure, and decreased exercise tolerance. To further assess potential alterations in ventricular function we have noninvasively studied diastolic performance in nine newly diagnosed and untreated hyperthyroid patients. Parameters including diastolic flow velocities, isovolumic relaxation time (IVRT), and the rate of diastolic flow deceleration were compared to those of an age- and sex-matched control population, and then repeat determinations were made after beta-adrenergic blockade and again when the patients were chemically and clinically euthyroid. Before treatment the IVRT was 33.0 ms, which was significantly (P less than 0.005) shorter than the control value (57.9 ms) and in combination with other measures of diastolic function indicated enhanced left ventricular relaxation. beta-Adrenergic blockade slowed the resting heart rate from 97 to 80 beats/min (P less than 0.005) and partially normalized the rate of diastolic deceleration, but had no effect on the IVRT (33.8 ms). When patients were euthyroid, the IVRT was 51.7 ms, and other measures of diastolic performance were the same as those in controls. The current data assessing resting diastolic function in hyperthyroidism are similar to those previously reported for systolic function. Our findings of enhanced cardiac diastolic performance do not support the hypothesis that thyrotoxicosis is associated with compromised left ventricular function and suggest the possibility that the cardiac symptoms that accompany hyperthyroidism may be due to noncardiac mechanisms.

Adult↗