Research

Chandrasegaram MD, Celermajer DS, Wilson MK

J Cardiothorac Surg 2007;2:14

PMID: 17313686

Abstract

BACKGROUND: Apical ballooning syndrome (or Takotsubo cardiomyopathy) is a syndrome of transient left ventricular apical ballooning. Although first described in Japanese patients, it is now well reported in the Caucasian population. The syndrome mimicks an acute myocardial infarction but is characterised by the absence of obstructive coronary disease. We describe a serious and poorly understood complication of Takotsubo cardiomyopathy.

CASE PRESENTATION: We present the case of a 65 year-old lady referred to us from a rural hospital where she was treated with thrombolytic therapy for a presumed acute anterior myocardial infarction. Four hours after thrombolysis she developed acute pulmonary oedema and a new systolic murmur. It was presumed she had acute mitral regurgitation secondary to a ruptured papillary muscle, ischaemic dysfunction or an acute ventricular septal defect. Echocardiogram revealed severe mitral regurgitation, left ventricular apical ballooning, and systolic anterior motion of the mitral valve with significant left ventricular outflow tract gradient (60-70 mmHg). Coronary angiography revealed no obstructive coronary lesions.She had an intra-aortic balloon pump inserted with no improvement in her parlous haemodynamic state. We elected to replace her mitral valve to correct the outflow tract gradient and mitral regurgitation. Intra-operatively the mitral valve was mildly myxomatous but there were no structural abnormalities. She had a mechanical mitral valve replacement with a 29 mm St Jude valve. Post-operatively, her left ventricular outflow obstruction resolved and ventricular function returned to normal over the subsequent 10 days. She recovered well.

CONCLUSION: This case represents a serious and poorly understood association of Takotsubo cardiomyopathy with acute pulmonary oedema, severe mitral regurgitation and systolic anterior motion of the mitral valve with significant left ventricular outflow tract obstruction. The sequence of our patient’s presentation suggests that the apical ballooning caused geometric alterations in her left ventricle that in turn led to acute and severe mitral regurgitation, systolic anterior motion of the mitral valve and left ventricular outflow tract obstruction. The left ventricular outflow tract obstruction and mitral regurgitation were corrected by mechanical mitral valve replacement. We describe a variant of Takotsubo cardiomyopathy with acute mitral regurgitation, systolic anterior motion of the mitral valve leaflet and left ventricular outflow tract obstruction of a dynamic nature.

Ghaffari SR, Sabokbar T, Mollahajian H, Dastan J, Ramezanzadeh F, Ensani F, Yarandi F, Mousavi-Jarrahi A, Mohagheghi MA, Moradi A

Asian Pac. J. Cancer Prev. 2006 Oct-Dec;7(4):529-32

PMID: 17250423

Abstract

INTRODUCTION: HPV infection has a prime etiologic role in development and progression of cervical cancer, one of the most frequent forms of cancer among women in developing countries. This study was designed to determine the most prevalent HPV genotypes in women with normal and abnormal cervical cytology in Iran.

MATERIALS AND METHODS: Samples from134 patients, including 127 who attended gynecology clinics and 7 with solid cervical tumors were used. All 127 patients underwent routine Pap tests for cytological evaluation and at the same visit a sample of cervical epithelial cells was obtained by scraping the cervix osteum. In each case HPV infection was primarily evaluated by PCR using GP 5/6 primers and then subtyping was performed in proved infected samples with specific primers for HPV 16, 18, 31, 33, 11 and 6. After cytological evaluation, 50 patients with abnormal Pap tests were categorized as the abnormal group and the remaining 77 patients as the normal group.

RESULTS: In the normal group, HPV infection was established in 10 cases (13% infection rate), while 30 HPV positive cases were discovered in the abnormal group (60% infected). The most prevalent genotypes among the infected samples were HPV 16 (76%), HPV18 (12.7%) and HPV11/6 (8.5%). Moreover, all 7 tumor samples were positive for HPV general primers of which, 5 samples were infected with HPV 16, two were co-infected with HPV16,18 and HPV16,31 genotypes and one was infected with HPV 18.

CONCLUSIONS: Infection with HPV 16 was found to be significantly higher in abnormal group in comparison with normal group (42% vs. 11.6%, P value <0.005), likewise HPV18 genotypes were proved to be more prevalent in abnormal group (8% vs. 0%, P value <0.05). No significant relation between other HPV genotypes and pathologic cervical changes was obtained. According to our study high rates of infection with HPV genotypes in sexually active Iranian women makes molecular investigation for HPV16 and 18 very essential in clinical approaches to patients with proven dysplasia in their screening tests and also for those patients with borderline (i.e. ASCUS) or incongruous pathology reports. Larger studies are required to determine the most appropriate vaccine with highest protection in Iranian women.

Lau GT, Ridley LJ, Bannon PG, Wong LA, Trieu J, Brieger DB, Lowe HC, Freedman BS, Kritharides L

Circulation 2006 Jul;114(1 Suppl):I435-40

PMID: 16820615

Abstract

BACKGROUND: The use of saphenous vein grafts (SVG) in coronary artery bypass surgery is established but little is known of SVG remodeling during the first year in vivo.

METHODS AND RESULTS: The feasibility of measuring total vessel diameter (lumen plus wall), lumen diameter, and wall thickness by a novel computed tomography (CT) method was established in phantom model tubes (r=0.98 for lumen diameter and r=0.98 for wall thickness) and in an initial clinical study of 14 patients correlating CT and intravascular ultrasound measurements of SVG (r=0.88 for total vessel diameter, r=0.85 for lumen diameter and r=0.89 for wall thickness). In a separate group of 42 patients (aged 66+/-10 years; 36 male, 6 female) undergoing coronary artery bypass grafting, SVG total vessel diameter, lumen diameter, and wall thickness were determined prospectively with multi-slice CT angiography at 1 and 12 months postoperatively. Mean total vessel diameter decreased from 5.95+/-0.83 mm to 5.39+/-0.87 mm, P5%. Mean lumen diameter decreased from 3.69+/-0.66 mm to 3.36+/-0.68 mm, P<0.001, (range, -40 to +11% change). Surprisingly, mean wall thickness decreased from 1.14+/-0.27 mm to 1.01+/-0.21 mm (P<0.001; range, -48 to +33% change).

CONCLUSIONS: Lumen loss in SVG between postoperative months 1 and 12 is predominantly caused by negative remodeling of the whole vessel rather than to changes in wall thickness. Therapies targeting negative remodeling may be required for optimal maintenance of SVG lumen in the first postoperative year.

Stanley N, Stadler N, Woods AA, Bannon PG, Davies MJ

Free Radic. Biol. Med. 2006 May;40(9):1636-43

PMID: 16632123

Abstract

Previous studies have provided compelling evidence for the presence of oxidized proteins and lipids in advanced human atherosclerotic lesions. The catalyst responsible for such oxidation is unknown and controversial. We have previously provided evidence for elevated levels of iron in lesions. In this study we hypothesized that if iron ions catalyzed protein and lipid oxidation in the artery wall, then there should be a positive correlation between these parameters. Iron concentrations in ex vivo healthy human arteries and advanced carotid lesions were quantified by electron paramagnetic resonance spectroscopy. Four specific side-chain oxidation products of proteins, and the lipid oxidation products 7-ketocholesterol and cholesterol ester alcohols and hydroperoxides, were quantified by HPLC in the same samples used for the iron measurements. Parent amino acids, cholesterol, and cholesterol esters were also quantified. Statistically elevated levels of iron, cholesterol, cholesterol esters, 7-ketocholesterol, and cholesterol ester alcohols and hydroperoxides were detected in advanced lesions compared with healthy control tissue. Iron levels correlated positively and strongly with all four markers of protein oxidation, but not with either marker of lipid oxidation. These data support the hypothesis that elevated levels of iron contribute to the extent of protein, but not lipid, oxidation in advanced human lesions.

Wilson MK, Granger EK, Preda VA

Heart Lung Circ 2006 Apr;15(2):143-5

PMID: 16412689

Abstract

Pulmonary hypertension as the initial presentation of occult malignancy is extremely rare. The differential diagnosis of pulmonary hypertension due to arterial tumour embolism is often overlooked and deserves contemplation. Our case report details the presentation of cardiorespiratory decompensation from an assumed classic saddle pulmonary embolus in a previously fit, well 80-year-old gentleman. The patient underwent successful pulmonary thromboendarterectomy, however, intraoperatively the specimen was noted to be atypical. This resulted in the surprising definitive diagnosis of thromboembolic pulmonary hypertension secondary to laminated thrombi of metastatic squamous cell tumour emboli. The site of tumour origin was however not histologically apparent and was unable to be elucidated on extensive further investigation. Post-operatively the patient had considerable subjective and functional improvement returning to activities of daily living. He however passed away some 9 months later.

McLeod NP, Vallely MP, Mathur MN

Heart Lung Circ 2005 Mar;14(1):45-7

PMID: 16352251

Abstract

We report a case of a massive mediastinal teratoma in an 18-year-old woman who presented with a short history of exertional dyspnoea. The tumor arose from the left lobe of the thymus and extended into the left pleural cavity, completely compressing the left lung and extensively shifting the mediastinum to the right. Measuring 23 cm x 17 cm x 9 cm and weighing 2005 g it is one of the largest anterior mediastinal teratomas reported. It was successfully treated by surgical resection, with a final pathological diagnosis of a grades 1-2 immature teratoma.

Nguyen-Do P, Bannon P, Leung DY

Ann. Thorac. Surg. 2004 Aug;78(2):e26-7

PMID: 15276584

Abstract

We report the case of a fistula formation between the left circumflex coronary artery draining into the left atrium as a complication of radiofrequency cardio-ablation and resection of the atrial appendages. This complication was diagnosed with the use of transesophageal echocardiography and was subsequently confirmed on coronary angiography.

Gan S, Bannon PG

ANZ J Surg 2003 Nov;73(11):966-7

PMID: 14616584

Abstract

Ryan JB, Hicks M, Cropper JR, Garlick SR, Kesteven SH, Wilson MK, Feneley MP, Macdonald PS

Transplantation 2003 Sep;76(5):766-71

PMID: 14501850

Abstract

BACKGROUND: The aim of this study was to determine the efficacy of cariporide (a sodium-hydrogen exchanger inhibitor), BMS180448 (a pharmacologic ischemic preconditioning agent), and the combination thereof, as adjuvant therapies for extended cardiac allograft preservation.

METHODS: A porcine model of donor brain death and orthotopic heart transplantation was used. All hearts were arrested and stored for 14 hr in an extracellular preservation solution. Control hearts (CON; n=3) did not receive any additional treatment. Treated hearts received BMS180448 alone (BMS; n=3), cariporide alone (CAR; n=6), or both BMS180448 and cariporide (B+C; n=6). Donors of BMS180448-treated hearts received 2 mg/kg, 15 min before explantation. Donors and recipients of cariporide-treated hearts received 2 mg/kg, 15 min before explantation and reperfusion, respectively.

RESULTS: The CON and BMS arms of the study were terminated after three transplantations because initial results in these groups were poor. Significantly, none of the control hearts could be weaned successfully from bypass, whereas all of the treated hearts were weaned successfully (CAR vs. CON and B+C vs. CON: P=0.012). The rate of troponin I release during the first 3 hr after reperfusion was significantly lower in CAR (P=0.0180) and B+C (P=0.0154) recipients than in CON recipients. Mean plasma troponin I levels (microg/mL) 3 hr after reperfusion were as follows: CON 633+/-177, BMS 576+/-110, CAR 346+/-93, and B+C 296+/-97.

CONCLUSION: In this porcine model of extended cardiac allograft preservation, cariporide was more effective than BMS180448 as an adjuvant to our usual preservation solution. There was no additional benefit from the combination of the two therapies.

Ryan JB, Hicks M, Cropper JR, Garlick SR, Kesteven SH, Wilson MK, Feneley MP, Macdonald PS

J. Heart Lung Transplant. 2003 Aug;22(8):922-8

PMID: 12909474

Abstract

BACKGROUND: Acute brain death from increased intracranial pressure results in a transient increase in myocardial adenosine and lactate, which indicates that oxygen demand exceeds oxygen delivery during the sympathetic “storm”. The aim of this study was to determine the functional significance of this period of ischemia.

METHODS: Brain death was inflicted on 40 Westran pigs (36.5-68.0 kg) by inflating a 21-ml subdural balloon over 3 minutes. In 38 animals, micromanometry and sonomicrometry were used to obtain left ventricular pressure-volume loops to determine the preload recruitable stroke work (PRSW) relationship. Data files were recorded before and at 15-minute intervals after beginning balloon inflation. Plasma troponin I was measured before and 60 minutes after beginning balloon inflation in the 38 instrumented and 2 non-instrumented animals.

RESULTS: All animals experienced the classical sympathetic storm. The slope of the PRSW relationship decreased, and the volume-axis intercept shifted to the right 15 minutes after beginning balloon inflation (p < 0.0001). Progressive incremental recovery (leftward shift) occurred between subsequent time points (p < or = 0.0018). In the instrumented animals, the mean plasma troponin I level increased from 1.4 +/- 1.6 microg/liter to 2.8 +/- 2.3 microg/liter (p < 0.001). However, troponin I was not detected before or after induction of brain death in the plasma of either non-instrumented animal (p = 0.001).

CONCLUSIONS: The sympathetic storm produced transient contractile dysfunction, consistent with ischemic injury. However, troponin I release reflected surgical instrumentation and not brain death.