J M Tharakan

Sree Chitra Tirunal Institute for Medical Sciences and Technology, Tiruvananantapuram, Kerala, India

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Publications (32)130.1 Total impact

  • 06/2015; 10(2). DOI:10.1016/j.gheart.2015.03.018
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    ABSTRACT: Coronary embolisation, spontaneous coronary artery dissection, and myocardial bridges are rare causes of Myocardial Infarction (MI) in the youth. Here, we report a young male who developed myocardial infarction at the age of 19. Investigations revealed that he had mitral stenosis, myocardial bridge, and angiographic features of healed coronary dissection.
    09/2013; 7(3):104-5.
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    ABSTRACT: The data of 51 patients (33 females) who underwent excision of left atrial (LA) myxoma were retrospectively reviewed for correlation of tumour size and electrocardiographic (ECG) findings. Mean age was 39.1 ± 15 years (range 9-53 years). The LA enlargement (LAE) on ECG was defined by standard criteria. The LAE in ECG in these patients did not correlate with echocardiographic LA dimensions or with the degree of left ventricular (LV) inflow obstruction. But it was found that the presence of LAE in ECG predicted maximum tumour dimension of >5 cm and correlated with the degree of mitral regurgitation (MR). The LAE in ECG disappeared following surgery in 87.5% of patients. The LA enlargement on ECG in a patient with LA myxoma signifies larger tumour size or the presence of significant MR but is not necessarily associated with an increased LA size or LV inflow obstruction.
    Indian Heart Journal 03/2012; 64(2):170-2. DOI:10.1016/S0019-4832(12)60055-8 · 0.17 Impact Factor
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    ABSTRACT: Rheumatic fever and rheumatic heart disease (RHD) are still important problems in developing countries. Secondary prophylaxis which is the most cost-effective method in preventing recurrences of rheumatic fever is fraught with problems of drug compliance. The utility of 500 mg once weekly azithromycin (AZT), an orally effective long-acting antibiotic was evaluated against oral penicillin (phenoxy methyl penicillin 250 mg twice daily) in this study. Forty-eight consecutive patients (44% males, mean age 29.4 years) with established RHD were randomised into two groups-26 patients received AZT and 22 received oral penicillin. Patients were evaluated at randomisation, at 1 month, 3 months, and 6 months, clinically, serologically and by throat swab culture. End points were absence of streptococcal colonisation, infection or fever at the end of 6 months. During the study, 4 patients (15.4%) in the AZT group developed sore throat and fever, had positive throat culture and positive serology indicating streptococcal infection. None satisfied the criteria for rheumatic fever reactivation. None in the oral penicillin group developed streptococcal infection. In conclusion, weekly 500 mg of AZT is not effective in the prevention of streptococcal throat infection compared to oral penicillin therapy in adult patients with established RHD.
    Indian Heart Journal 01/2012; 64(1):12-5. DOI:10.1016/S0019-4832(12)60004-2 · 0.17 Impact Factor
  • Journal of Cardiovascular Electrophysiology 05/2011; 23(2):223-4. DOI:10.1111/j.1540-8167.2011.02080.x · 2.88 Impact Factor
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    Journal of the American College of Cardiology 04/2011; 57(14). DOI:10.1016/S0735-1097(11)61382-X · 15.34 Impact Factor
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    ABSTRACT: Selecting the device size using a sizing balloon could oversize the ostium secundum atrial septal defect (OSASD) with floppy margins and at times may lead to complications. Identifying the firm margins using trans-esophageal echocardiography (TEE) and selecting appropriate-sized device optimizes ASD device closure. This retrospective study was undertaken to document the safety and feasibility of device closure without balloon sizing the defect. Sixty-one consecutive patients who underwent trans-catheter closure of OSASD guided by balloon sizing of the defect and intra procedural fluoroscopy (group I) and 67 consecutive patients in whom TEE was used for defect sizing and as intraprocedural imaging during device deployment (group II) were compared. The procedural success rate, device characteristics, and complications were compared between the two groups. The procedure was successful in 79.7 % patients. The success rate in group II (60 of 67, 89.6%) was significantly higher than in group I (41 of 61, 67.2 %) (P = 0.002). Mean upsizing of ASD device was significantly lower in group II (P < 0.001). TEE also provided better success rate with smaller device in subjects with large ASD (>25 mm) and in those who were younger than 14 years of age. There were four cases of device embolization (two in each group); of which one died in group II despite successful surgical retrieval. Balloon sizing may not be essential for successful ASD device closure. TEE-guided sizing of ASD and device deployment provides better success rate with relatively smaller sized device.
    Annals of Pediatric Cardiology 03/2011; 4(1):28-33. DOI:10.4103/0974-2069.79619
  • S Harikrishnan · K Remash · Krishnakumar Nair · J M Tharakan
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    ABSTRACT: Intercoronary artery continuity is a rare variant of coronary circulation. Here we report a case where we found an intercoronary communication between the left and the right coronary artery. Right coronary angiogram showed filling of the left coronary artery and the left coronary angiogram showed filling of the distal right coronary artery, demonstrating bidirectional flow. The coronary arteries were free of atherosclerotic occlusive disease. The case is reported for its rarity.
    Indian Heart Journal 01/2010; 62(2):181-2. · 0.17 Impact Factor
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    S Harikrishnan · V K Ajithkumar · J M Tharakan
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    ABSTRACT: Spontaneous coronary artery dissection is a rare cause of myocardial infarction and sudden cardiac death. A 32-year-old man presented with effort angina. He had a positive treadmill exercise electrocardiogram test, and coronary angiography showed that he had dissection of all major coronary vessels. The left anterior descending coronary artery was completely blocked, probably secondary to dissection and subsequent occlusion. He was advised to undergo coronary artery bypass surgery, to which he did not agree; instead, he was treated by medication and followed up.
    The Canadian journal of cardiology 04/2007; 23(4):313-4. DOI:10.1016/S0828-282X(07)70761-4 · 3.94 Impact Factor
  • N Krishnakumar · S Harikrishnan · J M Tharakan
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    ABSTRACT: A 33-year-old male with idiopathic restrictive cardiomyopathy had dilated and tortuous veins over both lower limbs and over the scrotum with multiple hyperpigmented scars. He was in the habit of puncturing the veins to let out blood during episodes of worsening of dyspnoea, thereby relieving dyspnoea by decreasing the preload.
    International journal of cardiology 02/2007; 114(1):135-6. DOI:10.1016/j.ijcard.2005.11.054 · 6.18 Impact Factor
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    ABSTRACT: To compare the immediate and long term results of percutaneous mitral valvotomy using metallic commissurotome and Inoue balloon in juvenile mitral stenosis. Inoue balloon technique for mitral commissurotomy (IBMC) is well established and carried out worldwide in the treatment of juvenile mitral stenosis. Percutaneous mitral metallic commissurotomy (PMMC) is reported to be a cheaper and effective alternative to balloon mitral commissurotomy. Thirty-three patients aged less than 20 years, who underwent PMMC, were compared with 33 age and sex matched control patients who underwent IBMC. Success of valvotomy, procedure related complications, and follow-up events of the two techniques were compared. Basal echocardiographic and hemodynamic data were similar in both groups. Procedural success was similar in both groups, 31/33. Complications like cardiac tamponade and mitral regurgitation (requiring or not requiring mitral valve replacement) were similar in both groups. On follow-up of more than 3 years, both groups had comparable hemodynamic parameters and restenosis rates. Both IBMC and PMMC are successful in providing relief from severe juvenile mitral stenosis in terms of gain in valve area and reduction in transmitral gradient. Both techniques have similar procedural success and complication rates. The long term follow-up results are comparable at follow-up of more than 3 years.
    Catheterization and Cardiovascular Interventions 03/2006; 67(3):453-9. DOI:10.1002/ccd.20666 · 2.40 Impact Factor
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    K Nair · H S Krishnan · J M Tharakan
    Heart (British Cardiac Society) 10/2005; 91(9):1214. DOI:10.1136/hrt.2004.051458 · 6.02 Impact Factor
  • S Harikrishnan · Santhosh Kumar Dora · J M Tharakan
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    ABSTRACT: Two siblings with features of Brugada syndrome are reported. One of them had permanent pacemaker implantation elsewhere where he was evaluated for recurrent syncope and diagnosed to have tri-fascicular block. He continued to have syncopal episodes and subsequently detected to have runs of polymorphic ventricular tachycardia picked up on a routine ECG. His sibling also was found to have features of Brugada syndrome.
    International Journal of Cardiology 08/2005; 102(3):539-41. DOI:10.1016/j.ijcard.2004.08.033 · 6.18 Impact Factor
  • S Harikrishnan · J Stigimon · J M Tharakan
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    ABSTRACT: Rare association of coronary artery aneurysms with intra cranial aneurysms is reported. Also, association of abdominal aortic coarctation with intracranial aneurysms is rare. A 70-year-old female presented with subarachnoid hemorrhage secondary to rupture of intracranial aneurysm. On evaluation, she was found to have intracranial aneurysms in the vertebral and basilar artery, coronary aneurysms and descending thoracic aortic coarctation. This association is unreported. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
    International Journal of Cardiology 04/2005; 99(2):329-30. DOI:10.1016/j.ijcard.2003.10.067 · 6.18 Impact Factor
  • S Harikrishnan · T Titus · J M Tharakan
    Journal of the American Society of Echocardiography 03/2005; 18(2):183-4. DOI:10.1016/j.echo.2004.08.009 · 3.99 Impact Factor
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    Santosh Kumar Dora · Jagan Mohan Tharakan · Ajith Kumar
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    ABSTRACT: Negotiating the pacing lead into the right ventricle via left superior vena cava, at times, can be difficult. We report two such cases in which pacing leads were introduced into the right ventricle via left superior vena cava, with the help of stylet tip shaped into a large pigtail loop.
    Indian Heart Journal 01/2004; 56(2):150-1. · 0.17 Impact Factor
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    ABSTRACT: Vosberg H, Waldmüller S, Sakthivel S, Abdul Vahab Saadi, Rakesh P G, Goloubenko M, Tharakan J M, Richard P, Schwartz K, Rajamanickam C. (2003) Novel deletions in MYH7 and MYBPC3 identified in Indian families with familial hypertrophic cardiomyopathy. Abstract No 180, Europ J of Heart Failure 2 (1): 35 supplements (2003)
    European Journal of Heart Failure 07/2003; 2(1):35. · 6.58 Impact Factor
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    ABSTRACT: Mutations causing familial hypertrophic cardiomyopathy (HCM) have been described in at least 11 genes encoding cardiac sarcomeric proteins. In this study, three previously unknown deletions have been identified in the human cardiac genes coding for beta-myosin heavy chain (MYH7 on chromosome 14) and myosin-binding protein-C (MYBPC3 on chromosome 11). In family MM, a 3-bp deletion in MYH7 was detected to be associated with loss of glutamic acid in position 927 (DeltaE927) of the myosin rod. In two other families (HH and NP, related by a common founder) a 2-bp loss in codon 453 (exon 16) of MYBPC3 was identified as the presumable cause of a translation reading frame shift. Taken together 15 living mutation carriers were investigated. Six deceased family members (with five cases of premature sudden cardiac death (SCD) in families MM and NP) were either obligate or suspected mutation carriers. In addition to these mutations a 25-bp deletion in intron 32 of MYBPC3 was identified in family MM (five carriers) and in a fourth family (MiR, one HCM patient, three deletion carriers). In agreement with the loss of the regular splicing branch point in the altered intron 32, a splicing deficiency was observed in an exon trapping experiment using MYBPC3 exon 33 as a test substrate. Varying disease profiles assessed using standard clinical, ECG and echocardiographic procedures in conjunction with mutation analysis led to the following conclusions: (1) In family MM the DeltaE927 deletion in MYH7 was assumed to be associated with complete penetrance. Two cases of reported SCD might have been related to this mutation. (2) The two families, HH and NP, distantly related by a common founder, and both suffering from a 2-bp deletion in exon 16 of MYBPC3 differed in their average phenotypes. In family NP, four cases of cardiac death were documented, whereas no cardiac-related death was reported from family HH. These results support the notion that mutations in HCM genes may directly determine disease penetrance and severity; however, a contribution of additional, unidentified factors (genes) to the HCM phenotype can-at least in some cases-not be excluded. (3) The deletion in intron 32 of MYBPC3 was seen in two families, but in both its relation to disease was not unequivocal. In addition, this deletion was observed in 16 of 229 unrelated healthy individuals of the population of the South Indian states of Kerala and Tamil Nadu. It was not seen in 270 Caucasians from Russia and western Europe. Hence, it is considered to represent a regional genetic polymorphism restricted to southern India. The association of the deletion with altered splicing in transfected cells suggests that this deletion may create a "modifying gene", which is per se not or only rarely causing HCM, but which may enhance the phenotype of a mutation responsible for disease.
    Journal of Molecular and Cellular Cardiology 07/2003; 35(6):623-36. DOI:10.1016/S1567-4215(03)90108-1 · 5.22 Impact Factor
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    ABSTRACT: Mutations causing familial hypertrophic cardiomyopathy (HCM) have been described in at least 11 genes encoding cardiac sarcomeric proteins. In this study. three previously unknown deletions have been identified in the human cardiac genes coding for beta-myosin heavy chain (MYH7 on chromosome 14) and myosin-binding protein-C (MYBPC3 on chromosome 11). In family MM, a 3-by deletion in MYH7 was detected to be associated with loss of glutamic acid in position 927 (DeltaE927) of the myosin rod. In two other families (HH and NP, related by a common founder) a 2-bp loss in codon 453 (exon 16) of MYBPC3 was identified as the presumable cause of a translation reading frame shift. Taken together 15 living mutation carriers were investigated. Six deceased family members (with five cases of premature sudden cardiac death (SCD) in families MM and NP) were either obligate or suspected mutation carriers. In addition to these mutations a 25-bp deletion in intron 32 of MYBPC3 was identified in family MM (five carriers) and in a fourth family (MiR, one HCM patient, three deletion carriers). In agreement with the loss of the regular splicing branch point in the altered intron 32, a splicing deficiency was observed in an exon trapping experiment using MYBPC3 exon 33 as a test substrate. Varying disease profiles assessed using standard clinical, ECG and echocardiographic procedures in conjunction with mutation analysis led to the following conclusions: (1) In family MM the DeltaE927 deletion in MYH7 was assumed to be associated with complete penetrance. Two cases of reported SCD might have been related to this mutation. (2) The two families, HH and NP, distantly related by a common founder, and both suffering from a 2-bp deletion in exon 16 of MYBPC3 differed in their average phenotypes. In family NP. four cases of cardiac death were documented, whereas no cardiac-related death was reported from family HH. These results support the notion that mutations in HCM genes may directly determine disease penetrance and severity; however, a contribution of additional, unidentified factors (genes) to the HCM phenotype can-at least in some cases-not be excluded. (3) The deletion in intron 32 of MYBPC3 was seen in two families, but in both its relation to disease was not unequivocal. In addition, this deletion was observed in 16 of 229 unrelated healthy individuals of the population of the South Indian states of Kerala and Tamil Nadu. It was not seen in 270 Caucasians from Russia and western Europe. Hence. it is considered to represent a regional genetic polymorphism restricted to southern India. The association of the deletion with altered splicing in transfected cells suggests that this deletion may create a "modifying gene", which is per se not or only rarely causing HCM. but which may enhance the phenotype of a mutation responsible for disease.
    ISHR, Europe Chapter; 06/2003
  • Cardiology 02/2003; 99(1):55-6. DOI:10.1159/000068442 · 2.04 Impact Factor