Rohit Manoj Kumar

Endovascular Repair of a Traumatic Axillary Artery Pseudoaneurysm

A 72-year-old woman was admitted to the trauma services of our hospital with a history of nonhealing fracture of the left humerus of 4 weeks’ duration. Her presenting complaint was severe pain in the left upper limb and progressive swelling in the left axillary region. On physical examination there was a pulsatile large swelling in the left axillary region measuring 18 9 22 mm on initial examination. Distal pulsation, i.e., brachial and radial pulsations, were present but feeble. The patient underwent color-coded Doppler ultrasound, which revealed continuous but reduced nonphasic flow in the left upper limb arteries, consistent with a proximal subtotal occlusion. In addition, a sonolucent area was noted deep to the axillary artery, at the site of a large branch vessel, with flow into a small adjacent sac, consistent with pseudoaneurysm of the axillary artery. CT scan of the left shoulder revealed a nonunion fracture of the upper end of the humerus with a hypoechoic mass lesion with resorption of bone in the surrounding area. CT angiography revealed a large pseudoaneurysm of the left axillary artery (Figs. 1, 2). Retrograde access was obtained through the left common femoral artery via a 7-Fr sheath. A left subclavian injection via a Judkins right 4.0 catheter revealed a large aneurysm of the axillary artery with a leaking jet from the axillary artery (Fig. 3). The segment of the axillary artery was crossed with a 0.035 guidewire. An 8 9 60-mm FLUENCY Plus vascular stent-graft (Bard Peripheral Vascular, Tempe, AZ) was positioned across the lesion (Fig. 4). As the large aneurysmal sac was compressing the distal segment of the artery, the stent was dilated with a 6 9 20-mm balloon. A check angiogram revealed complete stoppage of the leak into the aneurysmal sac and a good distal pulse (Fig. 5). The aneurysm regressed in size postprocedure and repeat Doppler of the left upper limb revealed a marked reduction in the size of the aneurysm.

Synergistic effect of angiotensin II type-1 receptor 1166A/C with angiotensin-converting enzyme polymorphism on risk of acute myocardial infarction in north Indians

Introduction: This first study from north India investigated the synergistic effect of AT1R 1166A/C with the ACE I/D polymorphism on risk of acute myocardial infarction (AMI). Materials and Methods: Traditional coronary risk factors, ACE I/D and AT1R 1166A/C polymorphism were analyzed in 350 patients with AMI and 350 matched controls. Results: In univariate analysis, hypertension (52.9% vs. 11.1%; OR=8.9; 95%CI 6.0–13.3), diabetes mellitus (16.0% vs. 0.6%; OR=33.1; 95%CI 8.0–137), smoking (43.7% vs. 20.9%; OR=2.9; 95%CI 2.1–4.1), family history of coronary artery disease (22.3% vs. 14.0%; OR=1.8; 95%CI 1.2–2.6), high body mass index (64.3% vs. 51.4%; OR=1.7; 95%CI 1.3-2.3), high waist–hip ratio (46.2% vs. 2.3%; OR=37; 95%CI 16–85.8) and AT1R 1166AC genotype (20.6% vs. 12%; OR=1.9; 95%CI 1.3–2.9) were associated with AMI. In multivariate analysis, all these factors were found to be independent risk predictors for AMI. Subjects carrying the AT1R 1166AC+CC and ACE ID+DD combined genotype showed a twofold increased association (OR=2.1; 95%CI 1.2–3.5) compared with the AT1R 1166AA–ACE II combined genotype. Patients who smoked and who carried the ACE ID+DD genotype had 2.4-fold (OR=2.4; 95%CI 1.5–3.8), and with the AT1R 1166AC+CC genotype had 15-fold (OR=14.9; 95%CI 5.2–42.8) increased risk of AMI compared with non-smoking non-carriers. Conclusions: The AT1R 1166A/C polymorphism has association with AMI among north Indian patients, particularly if integrated with ACE I/D polymorphism and smoking.

Association of thrombomodulin gene polymorphisms and plasma thrombomodulin levels with acute myocardial infarction in north Indian patients.

This is the first study from north India that investigated the association of thrombomodulin (TM) polymorphisms with acute myocardial infarction (AMI) in 350 patients (≤ 40 years, n = 184 and ≥ 60 years, n = 166) and 350 matched-controls. The TM polymorphisms were determined by polymerase chain reaction–single-stranded conformational polymorphism and DNA sequencing. The TM 1418TT genotype (odds ratio [OR] 2.8; 95% confidence interval [CI] 1.3-6.4; P = .012) was independent risk predictor of young AMI as were hypertension (OR 3.3; 95% CI 1.8-5.9; P < .001), diabetes mellitus (OR 14.3; 95% CI 2.9-44.6; P = .001), smoking (OR 13.8; 95% CI 7.7-24.7; P < .001), family history (OR 1.8; 95% CI 1.1-3.3; P = .045), high body mass index (OR 2.2; 95% CI 1.3-3.6; P = .002), and high waist–hip ratio (OR 4.1; 95% CI 2.4-7.1; P < .001). Mean plasma TM also showed association with young AMI (P < .001). Smoking carriers of TM 1418CT + TT genotype had significantly higher risk of AMI (OR 12.8; 95% CI 6.0-27.3; P < .001) when compared with nonsmoking noncarriers. In conclusion, TM 1418C/T polymorphism is independent predictor of AMI and synergies with smoking.

Decreased Myocardial Expression of Dystrophin and Titin mRNA and Protein in Dilated Cardiomyopathy: Possibly an Adverse Effect of TNF-α

Background and aimsWhile the molecular basis of dilated cardiomyopathy (DCM) remains uncertain, concrete evidence is emerging that sarcomeric and cytoskeleton gene expression of myocardium isolated from failing versus non-failing patients differ dramatically. The central aim to this work was to find out the possible role of dystrophin and titin along with the TNF-α in the pathogenesis of cardiomyopathy.Patients and methodsmRNA levels and protein expression of a cytoskeletal protein, dystrophin and a sarcomeric protein, titin in endomyocardial biopsies of DCM patients were examined using RT-PCR and immunohistochemistry, respectively. Further, we examined the effect of TNF-α on myocardial expression of titin and dystrophin in vitro in rat cardiac myoblast cell line (H9c2).ResultsWe observed significantly decreased mRNA and protein levels of dystrophin and titin in endomyocardial biopsy of DCM patients as compared to control group. The decreased levels of these proteins correlated with the severity of the disease. Plasma levels of both TNF-α and its soluble receptors TNFR1 and TNFR2 were found to be significantly higher in patients as compared to control group. Treatment of H9c2 cells with TNF-α resulted in a dose- and time-dependent decrease in mRNA levels of dystrophin and titin. Pretreatment of these cells with MG132, an inhibitor of nuclear factor kappa B (NF-κB) pathway, abolished TNF-α-induced reduction in mRNA levels of dystrophin and titin.ConclusionOur results suggest that reduced expression of dystrophin and titin is associated with the pathophysiology of DCM, and TNF-α may modulate the expression of these proteins via NF-κB pathway.

Adhesion molecule expression and ventricular remodeling in chronic rheumatic heart disease: a cause or effect in the disease progression — a pilot study

BACKGROUND Rheumatic fever and chronic rheumatic heart disease (RHD) remains one of the most important causes of cardiovascular morbidity leading to a major public health problem, especially in developing countries. This was a pilot study to assess the presence of inflammation and expression of adhesion molecules by immunohistochemistry (IHC) in endomyocardial biopsy specimens of patients with chronic RHD. METHODS Endomyocardial biopsy was obtained from 14 patients of chronic RHD with no features of activity clinically. Biopsies were processed for histology and IHC. IHC was carried using monoclonal antibodies against CD3, CD4, CD8, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1. RESULTS Histomorphologically, varying degree of interstitial and perivascular fibrosis was seen in all the 13 patients (100%). Mild fibrosis (1+) was seen in five patients (38.5%); moderate interstitial fibrosis (2+) was present in four patients (30.8%).There was no Aschoff nodule or evidence of active myocarditis in any of the biopsy specimens. IMMUNOHISTOCHEMISTRY: Moderate positivity of (2+) and intense positivity of (3+) for intercellular adhesion molecule-1 was seen in 11 and 2 patients, respectively. With vascular cell adhesion molecule-1, four showed mild positivity (1+), and three showed intense positivity (3+). The phenotypic analysis of the inflammatory cells in our study revealed CD8(+) cells in 77%, CD4(+) in 23.1%, and CD3(+) in 38.5% of total patients, which suggests chronicity. CONCLUSION The nonspecific histomorphological changes and increased adhesion molecules expression could be a part of the ventricular remodeling due to the hemodynamic stress by the stenotic or regurgitant lesions of RHD itself.

Clinical Pearls in Pediatric Cardiology

In this section, the authors present four interesting clinical cases that presented with common symptoms, but required careful clinical examination and investigations to arrive at a correct diagnosis and institute appropriate management. The first case is a 3-month-old infant who presented with hypertonia, bulging anterior fontanelle and tachycardia. ECG revealed supraventricular tachycardia which was managed appropriately. The clinical suspicion of meningitis was not borne out by the CSF findings. The second is a pre-school girl who presented with recurrent, episodic wheezing that did not respond to standard asthma therapy. The authors discuss the management approach in such cases; careful examination of radiographs and clinical course led to the correct diagnosis of dilated cardiomyopathy. The next two cases are older children; one of them presented with massive bilateral pleural effusion; this was found to be caused by congestive cardiac failure. The last case is a 10-year-old child presenting with features of right sided heart failure without obvious cardiac abnormality on clinical examination. Advanced investigations confirmed a rare diagnosis of arrhythmogenic right ventricular dysplasia; retrospective ECG examination showed the characteristic findings of this condition.

An uncommon cause of a vascular mass in the left lung in neonate: A case report with a brief review of literature

A 20‐day‐old female child presented with mild respiratory distress since first week of life. On examination there was an ejection systolic murmur at left sternal border. Chest x‐ray revealed well‐defined mass in the left lung. Echocardiogram showed features suggestive tetrology of fallot with absent pulmonary valve with massively dilated main and left pulmonary artery. We report a rare cause of vascular mass in a neonate due to tetrology fallot with absent pulmonary valve. Pediatr Pulmonol. 2008; 43:822–823.

Genetic polymorphisms, Biochemical Factors, and Conventional Risk Factors in Young and Elderly North Indian Patients With Acute Myocardial Infarction.

This study compared genetic polymorphisms (factor V Leiden [FVL] 1691G/A, factor VII [FVII] 10976G/A, FVII HVR4, platelet membrane glycoproteins GP1BA 1018C/T, GP1BA VNTR, integrin ITGB3 1565T/C, ITGA2 807C/T and methylenetetrahydrofolate reductase [MTHFR] 677C/T), biochemical (fibrinogen and homocysteine), and conventional risk factors in 184 young and 166 elderly north Indian patients with acute myocardial infarction (AMI). Univariate analysis revealed higher prevalence of hypertension and obesity in elderly patients while smoking, alcohol intake, and low socioeconomic status in young patients (P < .001). Although mean fibrinogen predominated (P = .01) in elderly patients, mean homocysteine was higher (P < .001) among young patients. Prevalence of hyperhomocysteinemia was greater in young than in elderly patients (odds ratio: 2.8, 95% confidence interval: 1.8-4.4, P < .001); however, genetic polymorphisms were equally prevalent in young and elderly patients. Multiple logistic regression analysis showed smoking (P < .001), alcohol intake (P = .046), and hyperhomocysteinemia (P = .001) to be associated with AMI in the young patients while hypertension (P = .006) in elderly patients. To conclude, smoking, alcohol intake, and elevated homocysteine are the risk factors for AMI among young while hypertension among elderly patients.

Thrombocytopenia as a presenting feature of Kawasaki disease: a case series from North India

Thrombocytosis is well described in children with Kawasaki disease (KD). We describe six children with KD who had thrombocytopenia at disease onset. This is an unusual finding and has clinical implications in the diagnosis of this condition.