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Dive into the research topics where Apichai Khongphatthanayothin is active.

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Featured researches published by Apichai Khongphatthanayothin.


Critical Care Medicine | 1999

Impact of respiratory syncytial virus infection on surgery for congenital heart disease: Postoperative course and outcome

Apichai Khongphatthanayothin; Pierre C. Wong; Yousef Samara; Christopher J. L. Newth; Winfield J. Wells; Vaughn A. Starnes; Anthony C. Chang

OBJECTIVESna) To describe the postoperative course and outcome of cardiac surgery in children with recent respiratory syncytial virus (RSV) infection; and b) to evaluate whether timing of surgery has any impact on the outcome.nnnDESIGNnRetrospective case series.nnnSETTINGnIntensive care unit and medical and surgical wards of a teaching pediatric hospital.nnnPATIENTSnTwenty-five children (aged 25 days to 3.5 yrs; median, 4 months) with congenital heart disease who had cardiac surgery within 6 months after RSV infection.nnnINTERVENTIONSnNone.nnnMEASUREMENTS AND MAIN RESULTSnWe reviewed the clinical course and outcome of all patients. The cardiac diagnoses included ventricular septal defect (n = 11), tetralogy of Fallot (n = 3), atrioventricular canal (n = 3), and others (n = 8). Thirteen patients had surgery during the same admission as RSV infection (group I), and 12 patients had surgery electively after being discharged to home after RSV infection (group II). Two patients in group I died; both of these patients had undergone total repair of tetralogy of Fallot within 2 wks after admission for RSV infection. Postoperative complications in group I patients included pulmonary hypertension (n = 5), adult respiratory distress syndrome (n = 1), tracheal stenosis (n = 1), left ventricular dysfunction (n = 1), pericardial effusion (n = 1), secondary bacterial or fungal infection (n = 7), and deep venous thrombosis (n = 1). Of all group I patients, the ones who were operated on early appeared to be at higher risk for complications, especially for postoperative pulmonary hypertension. No patient in group II died, and only two patients had minor complications (one had reactive airway disease, and the other had a transient superior vena cava syndrome after a bidirectional Glenn operation).nnnCONCLUSIONSnCardiac surgery performed during the symptomatic period of RSV infection is associated with a high risk of postoperative complications, especially postoperative pulmonary hypertension. These complications appeared to be more frequent and of greater severity in patients who had earlier surgery compared with those who had later surgery. More studies are needed regarding the proper timing of cardiac surgery in patients with congenital heart disease and RSV infection.


The Journal of Pediatrics | 1998

Effects of cisapride on QT interval in children

Apichai Khongphatthanayothin; John Lane; Daniel W. Thomas; Lilly Yen; Donald Chang; Beth Bubolz

Abstract Recent reports of torsade de pointes and heart block associated with prolonged QT interval in children receiving cisapride raise questions about its safety. We prospectively examined the effects of cisapride on the QT interval in children. Electrocardiography was performed on 30 children before and after cisapride was administered. An additional 71 children underwent electrocardiography only after starting cisapride. The incidence of a corrected QT (QTc) interval >440 msec or a marked abnormality in T wave morphology was determined in all 101 children. Cisapride significantly lengthened the QTc with a mean increase of 15.5 ± 4.6 msec (mean ± SEM, p = 0.002) in the 30 children with baseline electrocardiographs. Twelve of the 101 patients were found to have a QTc >440 msec, and one had a new prominent notched T wave in all leads. In these 13 (13%) patients with repolarization abnormalities, other factors that might contribute to a long QT were noted in 11 (85%) patients. We conclude that cisapride use in children is associated with a modest increase in QT interval. The incidence of QTc >440 msec is low. Most children with long QTc have other factors that could compound the effects of cisapride. (J Pediatr 1998;133:51-6)


Journal of Cardiovascular Electrophysiology | 2000

Nonfluoroscopic Three‐Dimensional Mapping for Arrhythmia Ablation: Tool or Toy?

Apichai Khongphatthanayothin; Erol M. Kosar; Koonlawee Nademanee

Arrhythmia Ahlation with Nonfluoroscopic 3D Mapping. Introduction: Conventional mapping and ablation rely on fluoroscopy, which can result in imprecise positioning of the ablation catheter and long fluoroscopic exposure times. We evaluated a nonfluoroscopic three‐dimensional mapping system, termed CARTO, and compared the results of ablation using this technique with those of conventional mapping.


Intensive Care Medicine | 2003

Hemodynamic profiles of patients with dengue hemorrhagic fever during toxic stage: an echocardiographic study

Apichai Khongphatthanayothin; Monnipa Suesaowalak; Sunthorn Muangmingsook; Parvapan Bhattarakosol; Chitsanu Pancharoen

ObjectiveTo study left ventricular performance and hemodynamic abnormalities during different stages of dengue hemorrhagic fever (DHF).Design and settingObservational study in a tertiary medical school hospital.PatientsTwenty-four patients with serologically confirmed diagnosis of dengue virus infection and DHF according to the WHO criteria.MethodsEchocardiography was performed during toxic, convalescent stages and at least 2xa0weeks after discharge (recovery). Left ventricular ejection fraction, rate-corrected velocity of circumferential fiber shortening adjusted for end-systolic meridional wall stress (VCFC/ESS) Z score, end-diastolic volume Z score, cardiac index, heart rate, mean arterial pressure, and total systemic vascular resistance (SVR) were compared between different stages of DHF.ResultsEjection fraction and VCFC/ESS were significantly lower during the toxic stage than after recovery. End-diastolic volume was low during toxic stage and returned to normal during convalescence and recovery. Cardiac index was low during the toxic stage due to decreased preload (low end-diastolic volume) and depressed left ventricular ejection fraction. Cardiac index remained subnormal during convalescence due to sinus bradycardia. Wide variation in heart rate during toxic stage resulted in a small, nonsignificant increase compared to recovery. With treatment, heightened SVR resulted in relatively normal mean arterial pressure throughout the course of the illness.ConclusionsThe mechanism of decreased cardiac output during toxic stage of DHF is complex. Decreased preload is accompanied by decreased left ventricular performance, and possibly a subnormal heart rate response in some patients.


Pediatric Critical Care Medicine | 2007

Myocardial depression in dengue hemorrhagic fever: prevalence and clinical description.

Apichai Khongphatthanayothin; Pornthep Lertsapcharoen; Pentip Supachokchaiwattana; Vidhawas La-orkhun; Aree Khumtonvong; Charoon Boonlarptaveechoke; Chitsanu Pancharoen

Objectives: To determine the prevalence of myocardial depression and its effect on the clinical severity in patients with dengue hemorrhagic fever. Design: Clinical study. Setting: King Chulalongkorn Memorial Hospital, Bangkok, Thailand. Patients: Ninety-one children (age 10.5 ± 2.9 yrs, male/female = 52/39) with serologically or polymerase chain reaction-proven dengue virus infection. Interventions: Left ventricular ejection fraction (EF) was measured. The proportions of patients with EF <50% were identified in patients with dengue fever (DF, n = 30), dengue hemorrhagic fever without shock (DHF, n = 36), and dengue shock syndrome (DSS, n = 25). Comparisons of clinical findings were made among DSS patients with depressed ventricular function (EF <50%), fair ventricular function (EF ≥50% and <60%), and good ventricular function (EF ≥60%). Serum troponin T was analyzed in nine patients. Measurements and Main Results: EF during toxic stage was significantly lower in patients with DSS than DHF, and lower in DHF than DF (p = .05) with rapid recovery within 24–48 hrs. EF <50% was found in 6.7%, 13.8%, and 36% of patients with DF, DHF, and DSS during the toxic stage, respectively (p = .01). DSS patients with poor ventricular function had significantly more tachycardia and hepatomegaly. While end-diastolic volumes were similarly reduced, patients with lower EF tended to have lower cardiac output, required more aggressive intravenous fluid resuscitation, developed larger pleural effusion, and had higher incidence of respiratory embarrassment. No patient had elevated troponin T level. Conclusions: Transient myocardial depression is not uncommon in patients with DSS. Cardiac dysfunction in children with DSS may contribute to the clinical severity and the degree of fluid overload in these patients.


Pediatric Cardiology | 2009

Serum Level of Soluble Intercellular Adhesion Molecule-1 Correlates with Pulmonary Arterial Pressure in Children with Congenital Heart Disease

Kanrawee Sungprem; Apichai Khongphatthanayothin; Patchara Kiettisanpipop; Chotivitayatarakorn P; Yong Poovorawan; Pornthep Lertsapcharoen

BackgroundEndothelial activation and vascular inflammation are thought to be the mechanisms of pulmonary hypertension. Increased expression of the intercellular adhesion molecule (ICAM-1) and raised serum level of its soluble form (sICAM-1) are found in various conditions associated with endothelial activation.MethodsSerum samples from 31 children (14 boys and 17 girls; age, 4.9xa0±xa04.6xa0years) with congenital heart disease (CHD) collected at the time of cardiac catheterization were analyzed for sICAM-1 level. Uni- and multivariable stepwise linear regression analyses were performed for the following variables against the sICAM-1 level: age, hemoglobin, serum creatinine, systemic arterial pressure (SAP), pulmonary arterial pressure (PAP), pulmonary blood flow (Qp) and resistance (Rp), systemic blood flow (Qs) and resistance (Rs), Qp/Qs, Rp/Rs, and pulmonary and systemic oxygen saturation.Results The sICAM-1 levels in children who had CHD with and without pulmonary hypertension were 411xa0±xa0110 and 344xa0±xa081xa0ng/ml, respectively (pxa0=xa00.11). In the univariable models, age, serum creatinine, systolic PAP, mean PAP, diastolic PAP, Rp, and Rp/Rs were significantly correlated with sICAM-1 level. In the multiple stepwise regression model, only mean PAP remained as an independent predictor of sICAM-1 level (rxa0=xa00.55; pxa0=xa00.002).ConclusionChildren with CHD and pulmonary hypertension had a trend toward elevated sICAM-1 compared with CHD children who had no pulmonary hypertension. A linear correlation was found between mean pulmonary arterial pressure and sICAM-1 level.


Annals of Tropical Paediatrics | 2011

Spectrum of cardiac rhythm abnormalities and heart rate variability during the convalescent stage of dengue virus infection: a Holter study

Vidhavas La-orkhun; Pentip Supachokchaiwattana; Pornthep Lertsapcharoen; Apichai Khongphatthanayothin

Abstract Background: Various minor cardiac rhythm abnormalities have been reported in patients with dengue virus infection. Previous studies have used only random electrocardiograms (ECG) to assess the incidence of cardiac arrhythmias, and the time when the ECGs were undertaken was not systematically defined. Objectives: To evaluate cardiac arrhythmias and heart rate variability in children with dengue virus infection during the convalescent stage using Holter monitoring. Methods: Overnight 18–24-hour Holter monitoring was performed in 35 children [mean (SD) age 11·7 (2·3) y] at least 24 hours after defervescence (on the last day of admission). In 17 patients, time- and frequency-domain short-term (5 minutes) heart rate variability (HRV) during the convalescent stage was also compared with the value obtained during the follow-up visit (at least 14 days after defervescence). Results: During the convalescent stage, cardiac rhythm abnormalities were found in ten patients (29%), including sinus pause (1), first-degree (2) and Mobitz type I second-degree AV block (Wenckebach) (3) and atrial (4) and ventricular ectopic beats (5). There was no relationship between the clinical severity of dengue virus infection (DF, DHF without shock and DSS) and the incidence of cardiac arrhythmia. There was no significant difference in the averaged RR interval, the time-domain HRV (SDNN, RMSSD, pNN 50) or frequency-domain HRV (LF, HF, LF/HF ratio) between the convalescent stage and at follow-up. Conclusion: Various benign bradyarrhythmias and ectopic beats are detected in patients with dengue virus infection during the convalescent stage.


Pacing and Clinical Electrophysiology | 2003

Roxithromycin Induced Torsade de Pointes in a Patient with Complex Congenital Heart Disease and Complete Atrioventricular Block

Worakan Promphan; Apichai Khongphatthanayothin; Kriangsak Horchaiprasit; Vichai Benjacholamas

We reported a 6‐year‐old girl who developed torsade de pointes (TdP) after taking roxithromycin. The patient had congenital complete heart block and complex cyanotic heart disease. Before taking roxithromycin, her corrected QT interval (QTc) was 0.39 second with a ventricular rate of 55–60 beats/min. Repetitive bursts of TdP with prolonged QT interval ( QTc = 0.55u2003 s ) developed after taking roxithromycin. After stopping the medication, her QT interval normalized ( QTc = 0.38u2003 s ). This case demonstrated the potential of roxithromycin in causing TdP especially in a patient with other risk factors for prolong QT interval and TdP. (PACE 2003; 26:1424–1426)


Emerging Infectious Diseases | 2013

Possible cause of liver failure in patient with dengue shock syndrome.

Apichai Khongphatthanayothin; Atchara Mahayosnond; Yong Poovorawan

To the Editor: We report a rare hepatic ultrasonograph finding for a patient with liver failure associated with dengue virus (DENV) infection. This finding might shed light on the pathogenesis of liver involvement in this disease. n nIn March 2006, a 10-year-old previously healthy boy was hospitalized for a 3-day history of fever, headache, and nausea/vomiting. Fever subsided on the day of admission, but the patient was in shock (blood pressure 80/40 mm Hg) and had gastrointestinal bleeding and hematuria. Physical examination showed an obese, confused patient with generalized petechiae and hepatomegaly. The initial diagnosis was dengue shock syndrome (DSS). The patient was intubated and received intravenous fluid infusion, packed red blood cells, ceftriaxone, sodium bicarbonate, and ranitidine before being transferred to King Chulalongkorn Memorial Hospital in Bangkok. The patient’s blood pressure increased to 130/90 mm Hg after the initial fluid resuscitation (28 mL/kg free flow), and systolic pressure remained at ≈130 mm Hg until transfer. n nLaboratory examinations found 14,930 leukocytes/mm3, hemoglobin 16.4 g/dL, hematocrit 48.2%, platelet 18,000/mm3, blood urea nitrogen 33 mg/dL, creatinine 1 mg/dL, sodium 128 mEq/L, potassium 6.2 mEq/L, chloride 91 mEq/L, total CO2 5 mEq/L, total bilirubin 6.9 mg/dL, direct bilirubin 3.9 mg/dL, aspartate transaminase 3,507 IU/L, alanine transaminase 2,775 IU/L, prothrombin time 43 seconds (international normalized ratio 3.4), and partial thromboplastin time 93.5 s (control 28.7 s). Blood and urine cultures showed negative results. Serum was positive for IgM against DENV. Unfortunately, we did not investigate other viral causes of liver failure. n nDSS with liver failure was diagnosed and treated with intravenous fluid, sodium bicarbonate, omeprazole, fresh frozen plasma, platelet transfusion, vitamin K, and recombinant factor VIIa concentrate (NovoSeven; Novo Nordisk, Bagsvaerd, Denmark). Despite stable blood pressure over the next 6 days, liver enzymes continued to rise with progressive jaundice (Technical Appendix). Hepatic ultrasonograph on the second day after admission showed totally reversed direction of portal venous blood flow away from the liver (Figure, panel A), becoming bidirectional on the following day and, finally, reverting to normal direction (although with low velocity) 3 days later (Figure, panel B). Despite improved hemodynamic status, progressive encephalopathy and gastrointestinal bleeding developed and were unresponsive to treatment. Six days later, the patient died of pulmonary hemorrhage and progressive respiratory failure. n n n nFigure n nUltrasonograph with Doppler image of the liver of a 10-year-old boy with liver failure associated with dengue virus infection. A) Day 2 of hospitalization, showing reversed direction of blood flow in the right branch of the portal vein (hepatofugal flow). ... n n n nDENV infection is one of the most prevalent emerging infectious diseases affecting children and one of the leading causes of liver failure in tropical countries (1,2). Although liver involvement in patients with dengue hemorrhagic fever is well known, the mechanism for DENV-induced liver injury is still a mystery. Liver autopsy specimens of terminal DSS patients generally showed massive or focal necrosis with little or no recruitment of polymorphonuclear cells or lymphocytes (3,4). Ultrasonograph images from patients with liver failure caused by acetaminophen poisoning or hepatitis B indicate increased portal vein flow and normal flow velocity to the damaged liver (5). Decreased portal vein flow velocity and reversal of the flow direction is seen in the terminal stage of hepatic cirrhosis and a few other conditions such as hepatic sinusoidal obstruction (hepatic veno-occlusive disease), arterioportal fistula, extrahepatic portal vein thrombosis, and hepatic venous outflow obstruction (6). This finding is unusual in other instances of toxin- or virus-induced liver failure and might contribute to the understanding of the mechanism of liver involvement in patients with DENV infection. n nWe previously reported increased portal vein congestion during the toxic stage of DENV infection (7). At defervescence, the portal vein was dilated and blood flow velocity was decreased. This finding is usually observed for patients with high resistance in the hepatic sinusoidal capillary network, such as those with liver cirrhosis, and is correlated with the degree of portal venous hypertension (8). We postulate that DENV infection of the liver might affect the sinusoidal endothelial or Kupffer cells in a way that causes obstruction to the hepatic sinusoidal capillary lumen resulting in decreased portal venous blood velocity and flow to the liver and, when severe, shunting of portal blood away from the liver (hepatofugal flow). Because portal venous blood comprises 75% of total hepatic blood (6), this condition coupled with decreased hepatic arterial blood flow as a consequence of shock might have led to severe and irreversible liver damage in this patient. This hypothesis can be further supported by a pathology study of the skin in patients with DENV infection, which showed endothelial swelling and extrusion of its plasma membrane into the capillary lumen, resulting in narrowing of the capillary lumen (9). Of note are the similarities between clinical findings in patients with DENV infection and sinusoidal obstruction syndrome such as hepatomegaly, ascites, right pleural effusion, swelling of the gall bladder wall, and decreased velocity or reversed direction of portal blood flow (10). n nIn conclusion, we report a case of liver failure from DENV infection with reversal of portal venous blood flow. We postulate that hepatic sinusoidal obstruction coupled with shock might be the underlying mechanism of liver failure in this disease. n nTechnical Appendix: nClinical and laboratory data for patient with liver failure associated with dengue virus infection. n nClick here to view.(55K, pdf)


Shock | 2005

Hepatosplanchnic circulatory dysfunction in acute hepatic infection: the case of dengue hemorrhagic fever.

Apichai Khongphatthanayothin; Pornthep Lertsapcharoen; Pentip Supachokchaiwattana; Patcharapa Satupan; Kriangsak Thongchaiprasit; Yong Poovorawan; Chule Thisyakorn

The mechanism of shock in patients with dengue hemorrhagic fever (DHF) has not yet been fully understood. In this study, we investigated the possibility of splanchnic venous pooling as a contributor for circulatory dysfunction in these patients. Ultrasonographic studies of portal vein and inferior vena cava were done in 45 patients with serologically or PCR-confirmed diagnosis of dengue virus infection. The size of portal vein and inferior vena cava, mean blood flow velocity in the right portal vein, and modified portal vein congestion index were compared between patients with dengue fever (DF, n = 20), DHF without shock (n = 14), and dengue shock syndrome (DSS, n = 11) during the toxic stage, convalescent stage, and at follow-up. The portal vein was significantly more dilated in patients with shock (DSS) than DHF without shock and than DF during the toxic and convalescent stages (P < 0.05), but not at follow-up. The change in the size of inferior vena cava followed the opposite trend (not statistically significant). Portal vein blood flow velocity was lower and congestion index was higher in shock cases (DSS) than DHF without shock and than DF at toxic and convalescent stages (P < 0.01). The differences disappeared at follow-up. Hepatosplanchnic venous pooling and/or dysfunction occur and correlate with the severity of circulatory derangement and shock in patients with DHF. The cause(s) and significance of hepatosplanchnic circulatory dysfunction in DHF and possibly other viral hepatic diseases deserve further study.

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Chotivitayatarakorn P

King Chulalongkorn Memorial Hospital

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Vichai Benjacholamas

King Chulalongkorn Memorial Hospital

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John Lane

University of Southern California

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Pierre C. Wong

Children's Hospital Los Angeles

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Daniel W. Thomas

University of Southern California

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