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Biomedical subjects

C T Ting

Publications and source records attributed to C T Ting.

At least 19 recordsLinked to original sources
PubMed1999

Differential coronary microvascular function in patients with left ventricular dysfunction of unknown cause--implication for possible mechanism of myocardial ischemia in early stage of cardiomyopathy.

To evaluate whether or not coronary microvascular dysfunction is associated with exercise-induced myocardial ischemia in left ventricular dysfunction of unknown cause, both the treadmill exercise test (TET) and coronary hemodynamics were studied in 20 patients with impaired left ventricular ejection fraction (<50% by radionuclide ventriculogram), normal cardiac size, normal coronary angiogram and no evidence of clinical heart failure. Ten subjects with atypical chest pain were studied as the control. Coronary hemodynamics were studied both at baseline and after dipyridamole infusion (0.56mg/kg, i.v. for 4'). There was no difference in age, gender, blood pressure, baseline great cardiac venous flow (GCVF) and coronary vascular resistance between ten patients with a positive TET and the other ten with a negative TET. At baseline, coronary sinus oxygen concentration was increased and myocardial oxygen consumption reduced in patients with a positive TET compared with those with negative a TET. After dipyridamole infusion, maximum GCVF (102+/-47 vs. 144+/-31 ml/min, P=0.027) and coronary flow reserve (2.31+/-0.49 vs. 3.00+/-0.61, P=0.012) were significantly reduced and minimum coronary vascular resistance was higher (1.00+/-0.42 vs. 0.63+/-0.12 mmHg/ml/min, P=0.016) in patients with a positive TET than in those with a negative TET. At follow-up, 40% of patients with a positive TET and 10% of those with a negative TET developed clinical heart failure with a dilated left ventricle during a period of 45 months. Thus, coronary microvascular function is heterogeneous in patients with left ventricular dysfunction of unknown cause. In some of them, coronary microvascular dysfunction could be related to the presence of exercise-induced myocardial ischemia, suggesting that similar pathophysiology underlies the early stage of dilated cardiomyopathy and syndrome X.

Adult↗
PubMed1999

Coronary artery aneurysms: A 25-patient study.

Coronary artery aneurysm is a rare disorder, characterized by abnormal dilatation of a localized portion or diffuse segments of the coronary artery. We studied clinical demographics, catheterization findings, and clinical outcomes in an Asian patient cohort with documented coronary artery aneurysms. Compared to a Caucasian adult population, our patient cohort had a lower incidence of coronary artery aneurysm (0.25% vs. 2.6%), and more patients with nonobstructive coronary artery aneurysms (70%); age, gender, and coronary distribution were comparable. The initial presentation of myocardial infarction occurred in five patients (5/17, 30%) with nonobstructive coronary artery aneurysms; however, none who were receiving preventive medications consisting of anticoagulant and antiplatelet agents subsequently developed myocardial infarction. We conclude that the incidence of coronary artery aneurysms with or without associated significant coronary stenosis seems to be lower in the Asian population. In contrast, the incidence of nonobstructive coronary artery aneurysms is considerably high and should not be thought of as a relatively benign disease entity if not treated with preventive medications. Rheumatoid arthritis-related vasculitis might be a cause of coronary artery aneurysm. Surgical intervention is based on the severity of coronary artery stenosis. The result of medical treatment has been compatible with long-term survival. Cathet. Cardiovasc. Intervent. 48:31-38, 1999.

Adult↗
PubMed1999

Insulin-like growth factor I improves cardiovascular function and suppresses apoptosis of cardiomyocytes in dilated cardiomyopathy.

To investigate how insulin-like growth factor I (IGF-I) modulates cardiovascular function and myocardial apoptosis in heart failure, the therapeutic effects of IGF-I were determined in a canine model of dilated cardiomyopathy. The animals were paced at 220 beats/min, and the left ventricular (LV) chamber became dilated after 2 weeks. A subset of paced dogs was treated with s.c. injections of IGF-I from week 3 to week 4. After 4 weeks of pacing, untreated paced dogs developed significant ventricular dysfunction. IGF-I-treated paced dogs showed better cardiac output, stroke volume, LV end-systolic pressure, and LV end-diastolic pressure. Moreover, pulmonary wedge pressure and systemic vascular resistance were increased in the untreated group and decreased in the IGF-I-treated group. IGF-I treatment was associated with less thinning of the ventricular wall. Compared with the controls, untreated paced dogs showed increased apoptosis of cardiac muscle cells, which was partially suppressed by IGF-I treatment. The myocardial apoptotic index was negatively related to the thickness of the ventricular wall and to cardiac output, suggesting that ventricular remodeling/dysfunction involves the occurrence of myocardial apoptosis. Due to the close resemblance between this experimental model of dilated cardiomyopathy and human heart failure, the results of this study provide evidence that IGF-I may be a potential therapeutic agent for the failing human heart.

Animals↗
PubMed1999

Changes of the insulin-like growth factor I system during acute myocardial infarction: implications on left ventricular remodeling.

In vitro and in vivo experiments have shown important biological actions of insulin-like growth factor I (IGF-I) in heart. The aims of this study were to determine the changes in circulating IGF-I and IGF-binding proteins (IGFBPs) during acute myocardial infarction (AMI) and to explore the relationship between IGF-I levels and myocardial remodeling and function after AMI. Thirty-four patients with acute Q-wave AMI and 17 matched controls were investigated in this study. Compared to normal subjects, free IGF-I and IGFBP-3 were significantly elevated, and IGFBP-1 was decreased upon AMI. Myocardial remodeling occurred after AMI in these patients. The day 2, 3, and 7 total IGF-I levels were inversely related to day 7 left ventricular (LV) end-diastolic, end-systolic diameters (r = -0.395 to -0.516) and LV mass (r = -0.487 to -0.661). Moreover, total IGF-I levels were positively related to LV ejection fraction (r = 0.402-0.453). Compared to the healthy survivors, those patients with poor outcomes had lower total IGF-I levels immediately after AMI. Most healthy survivors had total IGF-I levels greater than 137 ng/mL, but all patients with poor outcome had total IGF-I levels less than 137 ng/mL. Thus, AMI is associated with significant alterations in the IGF-I system. A higher total IGF-I level immediately after the onset of AMI is associated with better myocardial remodeling and ventricular function.

Echocardiography, Doppler↗
PubMed1999

Evaluation of arterial compliance in patients with carotid arterial atherosclerosis.

BACKGROUND: High-resolution peripheral vascular sonography has the capability to determine vessel compliance. A number of factors affect compliance in humans, including age, hypertension and atherosclerosis. However, compliance in patients with coronary artery disease (CAD) combined with carotid artery lesions has not been well studied. The objectives of this study were: 1) to determine whether carotid artery compliance is reduced in patients with CAD and carotid artery lesions, and 2) to determine whether decreased arterial compliance is related to an abnormality in vascular wall structure. METHODS: The study participants included 12 patients with CAD and carotid artery disease (group III), 13 patients with CAD only (group II) and 13 age-matched normal subjects who served as controls (group I). High-resolution peripheral vascular ultrasonography was performed to directly visualize the common carotid artery and to measure its diameter and wall thickness. Carotid artery elastic properties were determined relative to arterial diameter and pressure generated within the heart. RESULTS: Carotid artery walls were thicker in Group II and III patients than in normal subjects (1.49 +/- 0.03 mm, 1.98 +/- 0.04 mm, vs 1.22 +/- 0.03 mm, p < 0.05 and p < 0.01). There were significant differences in wall thickness between subgroups of CAD patients (p < 0.01). Carotid distensibility was lower (21.8 +/- 1.2 x 10(-6).N-1.m2, 14.8 +/- 1.7 x 10(-6).N-1.m2, vs 25.6 +/- 1.5 x 10(-6).N-1.m2; p < 0.05 and p < 0.01) and Young's modulus of elasticity was higher (3.12 +/- 0.43 x 10(5).Nm-2, 4.18 +/- 0.30 x 10(5).Nm-2, vs 2.34 +/- 0.23 x 10(5).Nm-2; p < 0.05 and p < 0.01) in group II and III patients than in normal subjects. These two indices of carotid artery compliance also differed between subgroups of CAD (p < 0.01). Increased wall thickness may occur secondary to changes in the architectural structure of the vessel wall, and these atherosclerotic changes lead to decreased compliance of arteries. CONCLUSION: The mechanical properties of the carotid arteries provide reliable information regarding changes caused by atherosclerosis.

Arteriosclerosis↗
PubMed1999

Unilateral pulmonary artery agenesis with presentation of hemoptysis: a case report.

Unilateral pulmonary artery agenesis (UPAA), a rare congenital anomaly frequently associated with other cardiovascular abnormalities, is usually diagnosed and surgically treated in childhood. Those who do not suffer other cardiac anomalies (isolated UPAA) have only minor or no symptoms and survive into adulthood. Isolated UPAA in adult patients may present as recurrent respiratory tract infection, dyspnea on exertion, hemoptysis or an incidental finding of an abnormal chest radiograph. We present the case of a 38-year-old man with a congenital absence of the right pulmonary artery (PA) and recurrent hemoptysis. The diagnosis was confirmed by cardiac catheterization, which disclosed an absence of the right PA and systemic collaterals to the right lung from the right internal thoracic artery and posterior intercostal arteries.

Adult↗
PubMed1998

A rapidly evolving homeobox at the site of a hybrid sterility gene.

The homeodomain is a DNA binding motif that is usually conserved among diverse taxa. Rapidly evolving homeodomains are thus of interest because their divergence may be associated with speciation. The exact site of the Odysseus (Ods) locus of hybrid male sterility in Drosophila contains such a homeobox gene. In the past half million years, this homeodomain has experienced more amino acid substitutions than it did in the preceding 700 million years; during this period, it has also evolved faster than other parts of the protein or even the introns. Such rapid sequence divergence is driven by positive selection and may contribute to reproductive isolation.

Amino Acid Sequence↗
PubMed1998

Parasympathetic withdrawal antedates dynamic myocardial ischemia in patients with syndrome X.

This study was to evaluate the dynamic changes in cardiac autonomic control preceding electrocardiographic (ECG) myocardial ischemia in patients with syndrome X. Twenty-four-hour ambulatory ECG was obtained in 34 consecutive patients in a drug-free state. Fourteen (41%) of them, aged 58.8+/-13.5 years, presented a total of 19 ischemic episodes, mean duration 12.4+/-19.8 min (ranged 1 to 90 min). Heart rate variability was measured for 24 h; for 3 min and 30 min before, and during the 15 min (in five 3-min intervals) immediately antedating ST segment depression; and for another 3 min after ST segment back to normal. There were significant progressive shortenings in sinus cycle lengths over the 30 min preceding myocardial ischemia (-30 vs -3 minute, 822+/-32 ms vs 637+/-23 ins, P<0.05; a decrement of 22.5%). The sinus cycle lengths lengthened after ischemia ceased. High frequency activity, pNNSO and rMSS.D. were significantly reduced from the -30 min baseline to a nidus in the last 3 min before ischemia (P<0.05), whereas low frequency band and low/high frequency ratio did not present significant change. These findings strongly argue that cardiac autonomic control, especially vagal withdrawal, is involved in the pathogenesis of dynamic myocardial ischemia in syndrome X.

Adult↗
PubMed1998

Which arterial and cardiac parameters best predict left ventricular mass?

BACKGROUND: Many cardiovascular and noncardiovascular parameters are thought to be determinants of left ventricular mass (LVM). Complicated interactions necessitate the simultaneous measurement and consideration of each to determine their individual and collective impact on LVM. We undertook such a comprehensive study. METHODS AND RESULTS: The influence of anthropometry, cardiac size and contractility, arterial structure and function, as well as indices of lifestyle, physical activity, and dietary salt intake on LVM (by two-dimensionally guided M-mode echocardiography) was analyzed in 1315 Chinese subjects who were either normotensive or had untreated hypertension. Effects of many cardiac and arterial factors were assessed. In univariate analysis, almost all measured noncardiovascular, cardiac, and arterial variables were significantly correlated with LVM. In multivariate linear regression analyses, when age, sex, body habitus, fasting serum C-peptide level, dietary salt, physical activity, and lifestyle were accounted for, the optimum multivariate linear regression main effects model had an adjusted model r2 of 0.740, with 98% of the model variance accounted for by the 5 independent determinants of LVM: stroke volume (49.6%), systolic blood pressure (30.7%), contractility (14.7%), body mass index (1.8%), and aortic root diameter (1.6%). Other proposed arterial indices were significant independent determinants of LVM only when blood pressure was removed from the model and, even then, these indices not only resulted in less powerful prediction but also accounted for only a very small percentage of the total variance of LVM. CONCLUSIONS: In a large population, we (1) confirmed that age, body habitus, and some indexes of arterial structure and function are independent determinants of LVM; (2) found aortic diameter to be an independent structural determinant of LVM; (3) demonstrated that the effects of the derived measures of arterial function were small and provided no better predictive power than blood pressure alone; and (4) showed that when the best measures of cardiac and vascular load were included, the single most potent predictor was an index of left ventricular size.

Adult↗
PubMed1998

Positive selection driving the evolution of a gene of male reproduction, Acp26Aa, of Drosophila: II. Divergence versus polymorphism.

The evolution of the gene for a male ejaculatory protein, Acp26Aa, has been shown to be driven by positive selection when nonsibling species in the Drosophila melanogaster subgroup are compared. To know if selection has been operating in the recent past and to understand the details of its dynamics, we obtained DNA sequences of Acp26Aa and the nearby Acp26Ab gene from 39 D. melanogaster chromosomes. Together with the 10 published sequences, we analyzed 49 sequences from five populations in four continents. The southern African population is somewhat differentiated from all other populations, but its nucleotide diversity is lower at these two loci. We find the following results for Acp26Aa: (1) The R: S (replacement : silent changes) ratio is significantly higher in the between-species comparisons than in the within-species data by the McDonald and Kreitman test. Positive selection is probably responsible for the excess of amino acid replacements between species. (2) However, within-species nucleotide diversity is high. Neither the Tajima test nor the Fu and Li test indicates a reduction in nucleotide diversity due to positive selection in the recent past. (3) The newly derived nucleotides in D. melanogaster are at high frequency significantly more often than predicted by the neutral equilibrium. Since the nearby Acp26Ab gene does not show these patterns, these observations cannot be attributed to the characteristics of this chromosomal region. We suggest that positive selection is active, but may be weak, for each amino acid change in the Acp26Aa gene.

Animals↗
PubMed1998

Differential glucose tolerance in dipper and nondipper essential hypertension: the implications of circadian blood pressure regulation on glucose tolerance in hypertension.

OBJECTIVE: The goals of this study were to compare glucose tolerance in dipper and nondipper hypertensive patients and to explore the cause of glucose intolerance in essential hypertension. RESEARCH DESIGN AND METHODS: A total of 50 patients <45 years old who had essential hypertension were recruited and studied by 24-h blood pressure monitoring and an oral glucose tolerance test (OGTT). Autonomic function was assessed with spectral analysis of heart rate variability RESULTS: Dipper hypertensive patients (n=25) had lower nocturnal blood pressure than nondipper (n=25) patients. During OGTT, postprandial glucose levels were higher in the nondippers at 0, 90, and 120 min (all P < 0.05). Nondippers had a higher fasting insulin/glucose ratio than was apparent in normal control subjects. Despite higher postprandial glucose levels, nondippers had lower postprandial insulin levels. These results suggest that nondippers were insulin resistant and that their pancreatic beta-cell function was impaired. For all patients, nocturnal reduction of blood pressure was inversely related to total glucose levels under the OGTT curve and was positively related to postprandial insulin levels. Daytime heart rate did not differ between the dippers and nondippers, but nocturnal heart rate was higher in the nondippers, suggesting that nocturnal sympathetic activities were higher among the nondippers. Spectral analysis of heart rate variability suggests that the nondippers had lower parasympathetic activities and unbalanced sympathetic/parasympathetic outflow. CONCLUSIONS: These findings indicate that nondipper hypertensive patients are more glucose intolerant than are dipper patients. The abnormalities of glucose metabolism in nondippers could be explained by insulin resistance and beta-cell dysfunction. The results of spectral analysis suggest that abnormal autonomic outflow may represent a possible link between hypertension and associated metabolic dysfunction.

Adult↗
PubMed1998

Dopamine and dobutamine have different effects on heart rate variability in patients with congestive heart failure.

BACKGROUND: Autonomic dysfunction plays an important role in the pathogenesis, treatment and prognosis of congestive heart failure (CHF). Sympathomimetic amines have been widely used in the treatment of CHF, but reports on their autonomic effects in CHF are rare. This study was designed to evaluate the effects of dopamine and dobutamine on cardiac autonomic function as assessed by heart rate variability (HRV). METHODS: Twenty patients with symptomatic CHF (systolic dysfunction) were enrolled. After recording one-hour baseline electrocardiographs (ECGs), patients were randomly selected for either dopamine (4 micrograms/kg/minute, Group A) or dobutamine (4 micrograms/kg/minute, Group B) treatment for three days. On the third day, a 24-hour ambulatory ECG was recorded and a tilt-table test was performed. Only furosemide and nitrates were allowed for adjunctive therapy. HRV was measured before and after treatment in both time and frequency domains. Frequency-domain HRV was also measured during head-up tilt. RESULTS: After treatment, all patients improved [New York Heart Association fraction (NYHA Fc) 3.7 to 2.0]. Group A patients had higher post-treatment 24-hour HRV than those in Group B. SDNN (standard deviation of the average normal RR intervals in the entire ECG recording), SDANN (standard deviation of the average normal RR intervals for all five minute segments of an entire ECG recording) and SDNN indices in Group A were significantly higher than in Group B (90 +/- 33 ms vs 41 +/- 12 ms, 78 +/- 32 ms vs 36 +/- 11 ms, and 37 +/- 19 ms vs 16 +/- 7 ms, respectively, all p < 0.05). rMSSD (the square root of the mean of the squared differences between adjacent normal RR intervals over the entire ECG recording) and pNN50 (percentage of differences between adjacent normal RR intervals that are greater than 50 ms computed over the entire ECG recording) were also higher in Group A patients, with borderline significance. All measurements of total frequency and low-frequency and high-frequency components tended to be higher in Group A than Group B, but this was only significant for total frequency amplitude (22.9 +/- 13.4 ms vs 10.9 +/- 6.1 ms, p < 0.05). Dopamine but not dobutamine treatment seems to restore the depressed circadian change in frequency-domain HRV classically seen in patients with CHF. The HRV change during head-up tilting did not differ between the two groups. Three patients in Group B showed non-sustained ventricular tachycardia on ambulatory ECG during the treatment period. CONCLUSIONS: Dopamine and dobutamine have comparable therapeutic effects in patients with CHF, but low-dose dopamine more favorably affects cardiac autonomic function.

Aged↗
PubMed1998

Prediction of right ventricular infarction from standard surface ECG in patients with inferior myocardial infarction.

BACKGROUND: Patients with inferior myocardial infarction (MI) have a 45% chance of having concurrent right ventricular infarction (RVI); of these, 5-10% suffer hemodynamic collapse. Immediate correct diagnosis and appropriate management of such patients is vital. ST-segment elevation in the right precordial V4 lead (V4R) has a high diagnostic value in identifying RVI, but this determination requires additional time and cost. An attempt was made to use a collection of patients' standard surface electrocardiograms (ECG) to find any available data to detect RVI and to lead to a new way to diagnose RVI. METHODS: Fifty patients (males/females, 44/6; mean age, 64.3 +/- 6.9 years) with acute inferior myocardial infarction were enrolled in a first group to develop new diagnostic criteria for RVI. As a first step, the ST-segment change in every standard surface ECG lead was analyzed and compared with corresponding changes in V4R. RVI was diagnosed by typical clinical symptoms (chest pain for more than 30 minutes, ST elevation > 0.1 mV and enzyme changes) accompanying ST elevation of more than 0.1 mV in V4R (by Lopez-Sendon criteria) and echocardiographic findings. RVI was diagnosed in 24 (48%) patients using ECG. The new criteria were then tested in a secondary group of 48 patients (males/females, 43/5; mean age, 65.5 +/- 7.9 years) with inferior MI. RESULTS: Analysis of these patients found that ST depression in lead I and aVL was a specific characteristic of RVI (I + aVL > 0.2 mV). This criterion was applied to another group of patients with acute inferior MI to check the predictive value (sensitivity, 94.7%; specificity, 89.7%; positive predictive value, 85.7%; negative predictive value, 96.3%). CONCLUSIONS: In patients with evolving inferior MI, standard surface ECG analyzed for this criterion could aid clinical recognition of concomitant RVI.

Aged↗
PubMed1997

Effects of short-term treatment of nicorandil on exercise-induced myocardial ischemia and abnormal cardiac autonomic activity in microvascular angina.

The underlying mechanisms of myocardial ischemia in microvascular angina may include endothelial dysfunction, abnormal smooth muscle tone, and abnormal autonomic control of coronary microvasculatures. This randomized, double-blind, placebo-controlled, crossover study was conducted to evaluate the effect of nicorandil (a nitrate-potassium channel opener) therapy on exercise-induced myocardial ischemia and cardiac autonomic activity in 13 patients with microvascular angina. After a 2-week placebo run-in period, patients were randomly assigned to the first 2-week treatment with nicorandil 5 mg tid or placebo, then crossed over to the second 2-week treatment after a 2-week washout period. Treadmill exercise tests and 24-hour ambulatory electrocardiogram monitoring were performed at the end of each treatment phase. The results showed that both time to 1-mm ST depression and total exercise duration were significantly prolonged with nicorandil treatment compared with placebo (p = 0.026 and 0.036, respectively). Maximum exercise ST depression also tended to be less with nicorandil treatment than with placebo (p = 0.083). Compared with 10 healthy control subjects, study patients had significantly reduced heart rate variability in both low- and high-frequency bands while receiving placebo. Nicorandil treatment did not change the altered heart rate variability in either time domain or spectral analysis. Systemic hemodynamics were also unchanged with nicorandil treatment. Thus, 2-week oral nicorandil therapy moderately improved exercise-induced myocardial ischemia without modifying the already altered cardiac autonomic activity, suggesting that nicorandil might have a direct vasodilatory effect on coronary microvasculatures in patients with microvascular angina.

Administration, Oral↗
PubMed1997

Incipient speciation by sexual isolation in Drosophila melanogaster: extensive genetic divergence without reinforcement.

The collection of Drosophila melanogaster from Zimbabwe and nearby regions (the Z-type) yield females who would not mate with the cosmopolitan D. melanogaster males (the M-type). To dissect the genetic basis of this sexual isolation, we constructed 16 whole-chromosome substitution lines between two standard Z- and M-lines. The results were as follows: (1) All substitution lines appear normal in viability and fertility in both sexes, indicating no strong postmating isolation. (2) The genes for the behaviors are mapped to all three major chromosomes with the same ranking and comparable magnitude of effects for both sexes: III > II >> X > or = 0 (III, II and X designate the effects of the three chromosomes). The results suggest less evolution on the X than on autosomes at loci of sexual behavior. (3) The genes for "Z-maleness" are many and somewhat redundant. Whole-chromosome effects for Z-maleness appear nearly additive and show little dominance. (4) In contrast, "Z-femaleness" has less redundancy as partial genotypes never exhibit full phenotypic effects. Epistatic interactions and incomplete dominance can sometimes be detected. (5) The extensive genetic divergence underlying sexual isolation has evolved in the absence of detectable reduction in hybrid fitnesses. Sexual selection has apparently been a driving force of multiple facets of speciation at the nascent stage without reinforcement.

Animals↗
PubMed1997

Histamine 2 receptor blocker-ranitidine and sinus node dysfunction.

BACKGROUND: Histamine 2 (H2) receptors were observed to be present in the sinus node. H2 receptor blockers could attenuate the histamine-induced increase in sinus rate and could thereby worsen sinus node dysfunction. However, the data pertaining to electrophysiological effects of H2 receptor blocker ranitidine on sinus node function are not available as yet, although bradycardia has been occasionally reported along with ranitidine. The present study evaluates the electrophysiological effects of ranitidine on sinus node function, and also determines the safety of administering ranitidine to patients suffering from sinus node dysfunction. METHODS: Thirty-nine patients with clinical diagnosis of sinus node dysfunction were selected for this study. Electrophysiological effects of intravenous injection of 150 mg ranitidine on sinus node function was evaluated. Tests were performed for 21 patients in the basal state (Group 1) and for 18 patients (Group 2) after autonomic blockade (propranolol 0.2 mg/kg, and atropine 0.04 mg/kg). The sinus cycle length (SCL), sinus node recovery time (SNRT), corrected sinus node recovery time (CSNRT), sinoatrial conduction time (SACT), atrio-His (AH) and His-ventricle (HV) intervals and blood pressure (BP) before and after ranitidine were analyzed. RESULTS: In Group 1, changes in SCL, SNRT, CSNRT, SACT, AH, HV and BP were not found to be significant. However, in Group 2, wherein the patients received ranitidine after autonomic blockade, it was observed that ranitidine significantly prolonged SCL (905.0 +/- 31.0 to 1000.0 +/- 40.0 msec, p = 0.001), decreased systolic BP (134.7 +/- 4.7 to 124.8 +/- 4.8 mmHg, p < 0.001), and diastolic BP (71.9 +/- 2.0 to 67.9 +/- 1.9 mmHg, p = 0.001), while the changes in SNRT, CSNRT, SACT, AH and HV were not significant. CONCLUSIONS: A clinical dose of 150 mg ranitidine must be administered by a slow intravenous infusion for at least 5 minutes in case of patients suffering from sinus node dysfunction. Continuous monitoring of BP and heart rate are necessary, especially in cases of autonomic denervation.

Adult↗
PubMed1997

Syndrome X: pathophysiology and clinical management.

The term "syndrome X" is now widely used to specify a group of patients with anginal chest pain, ischemia-like electrocardiogram, normal coronary angiograms, and no evidence of coronary spasm. Though chest pain and exercise-induced myocardial ischemia may both be present in patients with syndrome X and those with coronary artery disease, the underlying pathogenesis of these two disease entities is different. In patients with syndrome X, the causes of angina and myocardial ischemia are multifarious while coronary angiograms are normal. Coronary microvascular function has been shown to be impaired in these patients. However, the presentation of myocardial ischemia may be varied and even subclinical, suggesting dynamic characteristics and regional distribution of coronary microvascular insufficiency in them. Recently, there is increasing evidence that chest pain may develop without detectable myocardial ischemia and has been attributed to abnormal pain perception in at least some of the patients. Thus, there is a heterogeneous group of patients with syndrome X. The rational patient management should be related to individual clinical presentation and depend upon the proper identification of the underlying mechanisms of anginal chest pain or myocardial ischemia or both in these patients.

Chest Pain↗