PubMed Health⌕ Search

Biomedical subjects

L Lind

Publications and source records attributed to L Lind.

At least 145 records · Page 8Linked to original sources
PubMed1995

Left ventricular hypertrophy in hypertension is associated with the insulin resistance metabolic syndrome.

OBJECTIVE: To investigate whether left ventricular hypertrophy is associated with the insulin resistance syndrome. METHODS: Fifty patients with untreated hypertension were evaluated by recording office blood pressure during regular antihypertensive treatment and 24-h ambulatory blood pressure and office blood pressure after 4-6 weeks on placebo, echocardiography with M-mode measurements of left ventricular wall thickness and pulsed-wave Doppler measurements of mitral flow in diastole and the hyperinsulinaemic euglycaemic clamp, for determination of insulin sensitivity. RESULTS: The left ventricular wall thickness was found to be significantly related to blood pressure [r = 0.44, P < 0.004 for 24-h ambulatory systolic blood pressure (SBP)], fasting insulin level (r = 0.32, P < 0.03) and haematocrit level (r = 0.37, P < 0.009) and inversely related to insulin sensitivity (r = -0.59, P < 0.0001). Multiple regression analysis with these relationships together with confounding factors age, sex, body mass index and waist: hip ratio as independent variables showed insulin sensitivity to be the only significant variable, explaining 43% of the variation in left ventricular wall thickness, whereas 24-h ambulatory SBP explained a further 7%. Left ventricular diastolic filling, as evaluated by the mitral Doppler early: atrial ratio, was significantly correlated with insulin sensitivity (r = 0.42, P < 0.003) and inversely related to blood pressure (r = -0.41, P < 0.02 for 24-h ambulatory SBP), left ventricular wall thickness (r = -0.34, P < 0.02) and serum fibrinogen level (r = -0.63, P < 0.0001). However, multiple regression analysis showed that insulin sensitivity was more closely related to diastolic filling than to blood pressure or left ventricular wall thickness. CONCLUSION: The present study showed left ventricular wall thickness to be closely associated with insulin resistance. Because diastolic dysfunction of the left ventricle was also related to a decreased insulin sensitivity, these findings suggest that left ventricular hypertrophy and diastolic dysfunction are associated with the insulin resistance metabolic syndrome.

Age Factors↗
PubMed1995

Metabolic effects of anti-hypertensive treatment with nifedipine or furosemide: a double-blind, cross-over study.

To evaluate the metabolic effects of two anti-hypertensive agents with different actions, nifedipine 20 mg twice daily and furosemide 60 mg twice daily, 23 patients with untreated essential hypertension performed a double-blind, cross-over study in treatment periods of 5 months. Metabolic effects were evaluated by serum lipoprotein determinations, the intravenous glucose tolerance test and the hyperinsulinaemic euglycaemic clamp technique. Nifedipine and furosemide reduced blood pressure to the same extent (-14 to -15 mm Hg for supine SBP and -9 to -10 mm Hg for supine DBP, both P < 0.0001). Whereas both drugs significantly increased the levels of glycolysated haemoglobin (HbA1c, +0.24%, P < 0.005 for nifedipine and +0.43%, P < 0.001 for furosemide), only furosemide increased fasting blood glucose (+0.3 mmol/L, P < 0.01) and fasting insulin (+2.2 mU/L, P < 0.05) but impaired the early insulin response to i.v. glucose (-15 mU/L, P < 0.05). Insulin sensitivity on the other hand was significantly impaired by nifedipine treatment only (-1.6 mg/kg/min, P < 0.01). Whereas treatment with nifedipine did not change serum lipids, furosemide caused an increase in serum cholesterol (+0.2 mmol/L, P < 0.05) because of a rise in the LDL fraction (+0.32 mmol/L, P < 0.001). The insignificant change in heart rate induced by nifedipine treatment correlated with the change in HbA1c (r = 0.50, P = 0.05) and was inversely related to the change in insulin sensitivity (r = -0.56, P < 0.05). In conclusion, both furosemide and nifedipine caused abnormalities in glucose metabolism. In the nifedipine group the effects on glucose metabolism were related to the occurrence of tachycardia suggesting that sympathetic nerve activation could be involved in the metabolic impairments.

Aged↗
PubMed1995

Is insulin resistance a predictor of the blood pressure response to anti-hypertensive treatment?

It is a general impression that the blood pressure (BP) response during monotherapy in hypertensive subjects is highly variable. As decreased insulin sensitivity is a frequent finding in hypertensive patients, the following study was performed to evaluate if the degree of insulin sensitivity could predict the BP response to different types of anti-hypertensive treatments. Insulin sensitivity was evaluated by the hyperinsulinaemic euglycaemic clamp technique before initiation of treatment with beta-adrenergic blockers (n = 181), thiazide diuretics (n = 60), ACE inhibitors (n = 73), non-dihydropyridine calcium antagonists (n = 38), dihydropyridine calcium antagonists (n = 26) or alpha-1 antagonists (n = 39) over periods of 3-6 months in hypertensive patients. The proportion of poor responders, defined as a reduction in the diastolic blood pressure (DBP) of < 3 mm Hg ranged between 8% and 30% in the different groups despite similar pretreatment DBPs (100-102 mm Hg). A decreased pretreatment insulin sensitivity was related to a poor DBP treatment response in the thiazide-treated group only (r = -0.33, P < 0.05). In this group also obesity, as evaluated by body mass index (BMI), was associated with a poor BP response (r = 0.28, P < 0.05), while obesity was a predictor of a favourable reduction in DBP in the group treated with non-dihydropyridine calcium antagonists (r = -0.34, P < 0.05). These associations were still significant when pretreatment DBP was taken into account in multiple regression analysis. Neither age nor sex were found to be significant predictors of BP response in any of the treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Prevalence of insulin resistance in essential hypertension.

OBJECTIVE: To establish the prevalence of insulin resistance in hypertensive subjects. DESIGN AND METHODS: The euglycaemic hyperinsulinaemic clamp was performed in 420 hypertensive patients taking no antihypertensive medication and in 51 age- and sex-matched healthy controls. No subjects with known diabetes mellitus or fasting hyperglycaemia were included in the study. RESULTS: The mean value for insulin-mediated glucose uptake (M-value at clamp) in the healthy control group (8.2 mg/kg per min) -2 SD was chosen as the cutoff limit for insulin resistance (4.4 mg/kg per min). At this cutoff limit, 27% of the hypertensive subjects were insulin resistant (mean value 3.1 mg/kg per min in this group, range 0.7-4.3). A similar prevalence of insulin resistance in hypertensive patients was found (31%) if the 95th percentile of the non-normally distributed insulin sensitivity index (M/I at clamp) was used to define the cutoff limit for insulin resistance: (4.4 mg/kg per min)/(mU/l x 100). In the insulin-resistant group, 50% showed elevated levels of serum triglycerides (> 2.0 mmol/l), 50% had abdominal obesity (waist:hip ratio > 0.95), 20% had elevated levels of serum uric acid (> 400 mumol/l) and 48% had low high-density lipid (HDL)-cholesterol levels (< 1.0 mmol/l). Half of the insulin-resistant hypertensives but only 20% of the non-insulin resistant group had two or more of these other four metabolic impairments (P < 0.001). Insulin resistance in hypertension was also associated with an increased heart rate (+3 beats/min faster than in non-insulin resistant hypertensive patients, P < 0.01), but no significant differences in blood pressure were found between insulin resistant and non-insulin resistant hypertensive patients. CONCLUSION: When insulin resistance was defined as an M-value at clamp of < 4.4 mg/kg per min, based on calculations from a healthy control sample, about 25% of a sample of hypertensive subjects, taking no antihypertensive treatment and with no history of diabetes mellitus or hyperglycaemia, was found to be insulin resistant. This group of insulin-resistant hypertensives also displayed a high degree of clustering of other metabolic impairments.

Adult↗
PubMed1994

The relationship of postoperative delirium with psychoactive medications.

OBJECTIVE: To examine the role of medications with known psychoactive properties in the development of postoperative delirium. DESIGN: Nested case-control study within a prospective cohort study. SETTING: General surgery, orthopedic surgery, and gynecology services at Brigham and Women's Hospital, Boston, Mass. PATIENTS: Cases (n = 91) were patients enrolled in a prospective cohort study who developed delirium during postoperative days 2 through 5. One or two controls (n = 154) were matched to each case by the calculated preoperative risk for delirium using a predictive model developed and validated in the prospective cohort study. MAIN OUTCOME MEASURES: Medication exposures were ascertained from the medical record by a reviewer blinded to the study hypothesis. Exposures to narcotics, benzodiazepines, and anticholinergics were recorded for the 24-hour period before delirium developed in the 91 cases and for the same 24-hour postoperative period for the 154 matched controls. RESULTS: Delirium was significantly associated with postoperative exposure to meperidine (odds ratio [OR], 2.7; 95% confidence interval [CI], 1.3 to 5.5) and to benzodiazepines (OR, 3.0; 95% CI, 1.3 to 6.8). Meperidine had similar associations with delirium whether administered via epidural or patient-controlled routes, although only the epidural route reached significance (OR, 2.4; 95% CI, 1.3 to 4.4; OR, 2.1; 95% CI, 0.4 to 10.7, respectively). For benzodiazepines, long-acting agents had a trend toward stronger association with delirium than did short-acting agents (OR, 5.4; 95% CI, 1.0 to 29.2; vs 2.6; 1.1 to 6.5), and high-dose exposures had a trend toward slightly stronger association than low-dose exposures (OR, 3.3; 95% CI, 1.0 to 11.0; vs 2.6; 0.8 to 9.1). Neither narcotics (OR, 1.4; 95% CI, 0.5 to 4.3) nor anticholinergic drugs (OR, 1.5; 95% CI, 0.6 to 3.4) were significantly associated with delirium as a class, although statistical power was limited because of the high use of narcotics and the low use of anticholinergics in the study population. CONCLUSIONS: Clinicians caring for patients at risk for delirium should carefully evaluate the need for meperidine and benzodiazepines in the postoperative period and consider alternative therapies whenever possible.

Aged↗
PubMed1994

Fine mapping of Best's macular dystrophy localizes the gene in close proximity to but distinct from the D11S480/ROM1 loci.

The Best's macular dystrophy (BMD) gene has previously been mapped to the 11q13 region. In this study, recombination data localizes the BMD gene to the 6-cM genetic interval between the markers Fc epsilon RI and D11S480/ROM1 in a large Swedish 12-generation BMD family. Mutation analyses of the candidate gene ROM1 did not reveal any mutations that could explain the disease phenotype. However, one recombination event between intragenic ROM1 polymorphisms and the BMD phenotype was detected. Therefore, it is highly unlikely that mutations in the ROM1 gene cause BMD. Identification of the disease gene will elucidate the pathophysiological mechanism in BMD, which may also be of importance in other retinopathies such as age-related macular degeneration.

Alleles↗
PubMed1994

On the interplay between insulin secretion and sensitivity as determinants of glucose tolerance.

Both insulin secretion and sensitivity have been claimed to be the main characteristics in the determination of future deterioration in glucose tolerance. In this cross-sectional study insulin secretion and insulin sensiturity were determined in 228 subjects with varying degrees of glucose tolerance. Insulin secretion was measured in an intravenous glucose tolerance test (IVGTT) and insulin sensitivity by the hyperinsulinaemic euglycaemic clamp test. Both the early insulin response in the IVGTT (increment) and the glucose disposal rate in the clamp test (M-value) were found to be related hyperbolically to fasting glucose (r = -0.63 and -0.66, respectively; both P < 0.0001) and in a second-order polynomial manner to the glucose disappearance rate (k-value) in the IVGTT (r = 0.53 and 0.48, respectively; both P < 0.0001). Multiple regression analysis showed the insulin increment in the IVGTT and the M-value in the clamp test to be equally important determinants of glucose tolerance, together explaining about 50% of the variation in fasting glucose and the k-value in the IVGTT. In conclusion, in this cross-sectional study insulin secretion and sensitivity studied over a broad range of glucose tolerance were found to be of almost equal importance in the determination of glucose tolerance. However, low levels of insulin increment in the IVGTT were more often associated with glucose intolerance than was a low insulin sensitivity.

Aged↗
PubMed1994

Metabolic gas exchange during gynaecological laparotomy and laparoscopy.

The purpose of this study was to evaluate metabolic gas exchange change during surgery performed with general anaesthesia. Metabolic gas exchange was measured continuously (Deltatrac) during 33 gynaecological laparotomies and 22 laparoscopies performed during anaesthesia with propofol, fentanyl and vecuronium in mechanically ventilated patients. In both groups of patients, oxygen consumption (VO2) increased rapidly after skin incision (5-8% after 5 min, P < 0.01) and further increased during the surgical procedure (7% at 15 min in the laparoscopy group, P < 0.001 and 15% at 60 min in the laparotomy group, P < 0.0001). Carbon dioxide production (VCO2), on the other hand, showed different patterns in the two groups. It is concluded that a dynamic development of VO2 was seen during surgery suggesting that continuous measurement of VO2 might be used to evaluate the metabolic response evoked by surgical intervention.

Adult↗
PubMed1994

Long-term metabolic effects of antihypertensive drugs.

In short-term studies (4 to 6 months) we have reported that antihypertensive treatment with beta-adrenergic blockade and thiazide diuretics induced insulin resistance, hyperinsulinemia, and a deranged lipid profile; the ACE inhibitor captopril increased insulin sensitivity without affecting serum lipids. In the present study, 65 of the original 149 patients with essential hypertension included in the short-term studies were reexamined after treatment for 2 to 3 years. The hyperinsulinemic euglycemic clamp method showed that the significant decrease in insulin sensitivity (p < 0.01) induced by treatment with pindolol, propanolol, metoprolol, atenolol, or hydrochlorothiazide after 4 to 6 months persisted after 2 to 3 years of treatment. Furthermore, the increase in insulin sensitivity reported for captopril after 6 months (p < 0.05) was not significantly altered during long-term treatment. Also, the raised levels of very low-density lipoprotein triglycerides (p < 0.01) and reduced levels of high-density lipoprotein cholesterol (p < 0.01) induced by most of the beta-adrenergic blockade without intrinsic sympathomimetic activity and hydrochlorothiazide persisted. Captopril, on the other hand, did not significantly affect the lipids during prolonged treatment. In conclusion, the magnitude of the metabolic effects induced by antihypertensive treatment during short-term studies was of the same order after long-term treatment over 2 to 3 years and were not significantly different from the results in the short-term studies.

Adrenergic beta-Antagonists↗
PubMed1994

Serum calcium and the ECG in patients with primary hyperparathyroidism.

Primary hyperparathyroidism (HPT) is associated with cardiovascular disease, but there are no systematic studies on the electrocardiographic findings in HPT. Preoperative electrocardiograms from 139 patients with primary HPT and 97 control patients were therefore investigated. Serum calcium levels were found to be significantly correlated to the QRS amplitude (r = .26, P < .002), ST-segment duration (r = -.55, P < .0001), QT interval (r = -.64, P < .0001), and T wave duration (r = .19, P < .009). These relations were still significant when the influence of age, sex, and blood pressure level were taken into account in the multiple regression analysis. Thus, the electrocardiograms from HPT patients, compared to normocalcemic control patients, showed a shorter duration of the ST-segment, representing the systolic interval, and an increased amplitude of the QRS complex, representing ventricular muscle mass. Furthermore, the duration of the T wave was significantly prolonged in HPT patients. The hemodynamic effects of these findings have to be further evaluated.

Aged↗
PubMed1994

Blood pressure reaction during the intraoperative and early postoperative periods in patients with primary hyperparathyroidism.

Hypertension is a well known finding in primary hyperparathyroidism (HPT). In the present study, systolic blood pressure (SBP) and heart rate were recorded before, during and after surgery for HPT in 101 patients (mean serum calcium 2.96 +/- 0.22 mmol/l) and compared to 91 scheduled general surgical patients matched for age, sex, duration of surgery and type of general anesthesia. The HPT patients displayed an increased mean SBP, given as mean +/- standard deviation, both before (147 +/- 28 vs 131 +/- 25 mm Hg in controls) and during surgery (142 +/- 24 vs 117 +/- 21 mm Hg in controls) as well as postoperatively (141 +/- 23 vs 118 +/- 17 mm Hg in controls, all p < 0.0001). The preoperative SBP was correlated to both the intraoperative and postoperative SBP (r = 0.59 and r = 0.61, both p < 0.00001). However, the blood pressure elevation during and after surgery was still significant (both p < 0.001) when corrected for the influence of the preoperative blood pressure level using multiple regression analysis. The heart rate was increased in the HPT subjects only in the postoperative period (88 +/- 12 vs 83 +/- 12 beats/min in controls, p < 0.007). In conclusion, the systolic blood pressure was found to be elevated both before, during and after surgery in HPT subjects when compared to a general surgical population. In the postoperative period, also the heart rate was increased in the HPT subjects. These findings suggest an increased cardiovascular response to surgical stress in HPT subjects.

Aged↗
PubMed1994

Influences of different antihypertensive treatments on indices of systemic mineral metabolism.

A negative calcium balance has previously been described in human hypertension with low levels of plasma ionized calcium (Ca2+) and an increased urinary excretion of calcium. The cause of this disturbance in mineral metabolism is not known, nor is it known if this derangement could be abolished if blood pressure is reduced by antihypertensive treatment. In the present investigation, the effects of antihypertensive monotherapy on serum and fasting urinary electrolytes were studied. For 3 to 6 months, 319 hypertensive patients entered 17 study groups, each group using one of the following antihypertensive drugs: dilevalol, metoprolol, antenolol, pindolol, propranolol, hydrochlorothiazide, bendrofluomethiazide, furosemide, spironolactone, doxazocine, prazocine, diltiazem, verapamil, nifedipine, isradipine, captopril, or lisinopril. Treatment with different beta-blockers, as well as diuretics, reduced the fasting urinary calcium excretion (P < .001). However, while the beta-blockers increased the proportion of the ionized form of calcium in blood (Ca2+) (P < .001), Ca2+ was further decreased by diuretic treatment (P < .05). Angiotensin converting enzyme inhibitors caused no major changes in mineral metabolism while of the calcium antagonists studied only verapamil raised the levels of Ca2+ (P < .01). No significant relationship between the changes in mineral metabolism and the reduction in blood pressure was observed in any of the treatment groups. Of the antihypertensive drugs used in the present study, beta-blockers appeared to reverse the basic abnormality with regard to calcium balance, suggesting that the activity of the sympathetic nerve system is involved in the disturbed calcium metabolism seen in hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed1994

Electrolyte changes and metabolic effects of lisinopril/bendrofluazide treatment. Results from a randomized, double-blind study with parallel groups.

The metabolic effects of lisinopril and bendrofluazide therapy were studied in 61 patients with essential hypertension in a randomized, double-blind study with parallel groups. The insulin sensitivity index, measured by hyperinsulinemic euglycemic clamp test, decreased by 22% (P < .01) during bendrofluazide treatment and by 15% (NS) during lisinopril treatment. The initial insulin response at intravenous glucose tolerance test (IVGTT) increased by 21% (P < .05) during lisinopril treatment but decreased by 13% (P < .05) during treatment with bendrofluazide, and in addition, the glucose disappearance rate decreased by 9% (P < .05) in the latter group. During oral glucose tolerance test (OGTT), the area under the glucose curve (AUCglucose) increased by 17% (P = .05) in the bendrofluazide-treated group but decreased by 19% (P = .05) in the lisinopril group, although there was no difference between the drug effects on AUCinsulin. The LDL/HDL cholesterol ratio increased during bendrofluazide treatment. The serum potassium concentration decreased by 10% (P = .0001) during bendrofluazide treatment but increased by 6% (P = .0001) in the lisinopril-treated group. The change in serum potassium was correlated to the change in initial insulin response and glucose disappearance rate at IVGTT, and inversely correlated to the change in AUCglucose at OGTT. In conclusion, alterations in serum potassium balance may affect the initial insulin release and glucose disposal. Bendrofluazide treatment decreases the serum potassium concentration, reduces the initial insulin release and the glucose disposal, and, in addition, impairs insulin sensitivity. Lisinopril treatment increases serum potassium concentration and the initial insulin response, and decreases AUCglucose, but does not improve insulin sensitivity per se.

Bendroflumethiazide↗
PubMed1994

The gene for diffuse palmoplantar keratoderma of the type found in northern Sweden is localized to chromosome 12q11-q13.

Hereditary palmoplantar keratoderma is characterized by hyperkeratosis of the skin of palms and soles. An autosomal dominant form of diffuse non-epidermolytic palmoplantar keratoderma, frequently complicated by fungal infections, is encountered in northern Sweden with a prevalence of 0.3-0.55%. We have examined two families with this type of palmoplantar keratoderma and localized the causative genetic defect to a 14 cM interval on chromosome 12q11-q13, a region known to contain the keratin type II gene cluster as well as the retinoic acid receptor gamma gene. The palmoplantar keratoderma variant investigated in this study is thus genetically different from epidermolytic palmoplantar keratoderma, which recently has been shown to result from mutations in the gene for the type I keratin 9.

Chromosome Mapping↗
PubMed1994

Localization of a gene for autosomal dominant amelogenesis imperfecta (ADAI) to chromosome 4q.

Amelogenesis imperfecta (AI), is an inherited odontological disease which affects the formation of enamel. We report a linkage analysis study performed on three Swedish families, where the affected members had an autosomal dominant variant of AI (ADAI) clinically characterized as local hypoplastic. Significant linkage to microsatellite markers on chromosome 4q were obtained. Recombinations localized the ADAI locus to a chromosome region which contains both a locus for the dental disorder dentinogenesis imperfecta and the albumin gene. Serum albumin has been suggested to play a role in enamel formation, and the albumin gene is therefore a candidate gene for this genetic disease.

Amelogenesis Imperfecta↗
PubMed1994

Metabolic effects of isradipine as monotherapy or in combination with pindolol during long-term antihypertensive treatment.

OBJECTIVES: To evaluate the effects of isradipine alone and in combination with pindolol on glucose and lipid metabolism during long-term antihypertensive therapy. DESIGN: Open long-term study with parallel groups. SETTING: Kungsgärdet Geriatric Hospital, Uppsala, a tertiary referral hospital. SUBJECTS: Twenty-six untreated hypertensive subjects. INTERVENTIONS: After 4 weeks on placebo, isradipine was titrated up to 10 mg daily to achieve appropriate blood pressure control (n = 11). If this failed, 5-10 mg pindolol was added. The treatments were continued for 2 years. MAIN OUTCOME MEASURES: Blood pressure, lipoprotein measurements, intravenous glucose tolerance test, hyperinsulinaemic euglycaemic clamp, HbA1c, body weight. RESULTS: Treatment with isradipine alone caused a sustained reduction in blood pressure (-22/-10 mm Hg, P < 0.01), but an increase in body weight (+2.2 kg, P < 0.05) and HbA1c (+1.5%; P < 0.001) were also noted. Addition of pindolol resulted in a similar degree of blood pressure reduction and weight gain, whilst HbA1c was less affected (+1.0%; P < 0.05, compared to isradipine alone). Insulin sensitivity became impaired in both groups (-1.2 to -1.5 mg kg-1 min-1; P < 0.01 for M-value at hyperinsulinaemic clamp) but after adjustment for the change in body weight the impairment was only significant (P < 0.01) in the group with combined treatment. The combined treatment also resulted in an increase in very-low-density-lipoprotein (VLDL) triglycerides (+ 0.37 mmol L-1; P < 0.05). CONCLUSIONS: The hypotensive effect of isradipine was sustained during long-term use but was associated with weight gain and an impaired glucose control. When isradipine was combined with pindolol there was also a reduction in insulin sensitivity and an increase in VLDL triglycerides, possibly as effects of the beta-adrenergic blockade.

Adult↗
PubMed1994

Cytoplasmic calcium regulation and the electrocardiogram in patients with primary hyperparathyroidism.

Primary hyperparathyroidism (HPT) is a disease caused by an abnormal cytosolic regulation of calcium concentration [Ca++]i leading to an increased secretion of parathyroid hormone and thereby increased levels of extracellular calcium. It is well known that the QT-interval measured at electrocardiography (ECG) is shortened in HPT subjects. Whether this is due to an abnormal intracellular handling of calcium also in the heart or to the raised extracellular calcium levels is not known. In order to study the extent to which the deranged extra- and intracellular levels of calcium in HPT patients were related to ECG characteristics, [Ca++]i was determined in vitro by microfluorometry in surgery-removed parathyroid cells at extracellular calcium concentrations of 0.5 mM and 30.0 mM and ECG was recorded preoperatively in 42 HPT patients and in 15 subjects operated on for atoxic goitre. Serum calcium and plasma-ionized calcium also were measured preoperatively. The QT-interval and ST-segment duration were both shortened in the HPT patients compared to controls (P < 0.001). [Ca++]i at 3.0 mM extracellular calcium divided by that at 0.5 mM was correlated to the QT-interval, when measured at the onset of the T-wave (QoT, r = 0.39, P < 0.03) and early diastolic phase (end of T-wave to onset of p-wave, r = -0.34, P = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗