Kikkeri Hemanna Setty Srinivasa

Dancing vegetations: Kocuria rosea endocarditis

We present images of a 35-year-old man with rheumatic mitral regurgitation. The patient presented with a 1 month history of continuous fever, worsened exertional dyspnoea and orthopnoea. With a clinical suspicion of infective endocarditis, the patient initially underwent a transthoracic echocardiogram, which revealed the possibility of vegetations attached to the mitral leaflets, though not definitively. In order to confirm the diagnosis, the patient was subjected to a transoesophageal echocardiogram, which showed an astounding image having multiple vegetations apparently dancing in …

Transesophageal Doppler Echocardiography Study of Pulmonary Venous Flow Pattern in Severe Mitral Stenosis and the Changes Following Balloon Mitral Valvuloplasty

The studies of pulmonary venous flow‐pattern in mitral stenosis (MS) have given conflicting data about the type of abnormality. This study was undertaken to assess the pulmonary venous flow‐pattern in severe MS and to study the changes occurring after balloon mitral valvuloplasty (BMV). There were 51 patients of MS with sinus rhythm with the mean age of 32.5 ± 9.35 years, 18 males and 33 females. Transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were performed before and after BMV. Pulmonary venous flow was recorded by TEE from left upper pulmonary vein (PV). Peak velocities (V) and velocity time integrals (VTI) of systolic wave (S), diastolic wave (D), and atrial reversal wave (A) were measured. The Sv/Dv and SVTIIDVTI were calculated. Mitral valve area (MVA) increased from 0.81 ± 0.18 cm2 to 2.02 ± 0.46 cm2, left atrium (LA) mean decreased from 28.55 ± 6.68 mmHg to 13.88 ± 4.89 mmHg, and cardiac output increased from 3.1 ± 0.86 L/min to 3.7 ± 1.02 L/min. The S, D, and A velocities increased from 33.84 ± 13.55 cm/s, 37.24 ± 11.55 cm/s, and 20.53 ±6.7 cm/s to 59.86 ± 18.25 cm/s, 48.43 ± 12.55 cmls, and 24.94 ± 9.14 cmls, respectively. The VTIs ofS, D, and A waves increased from 4.88 ± 2.24 cm, 6 ± 2.45 cm, and 2 ± 0.88 cm to 10.46 ± 4.23 cm, 8.82 ± 3.61 cm, and 2.34 ± 1.29 cm, respectively. MS leads to reduction in pulmonary flow velocities during all the phases. Successful BMV resulted in improvement of all these velocities, with improvement in systolic fraction being the maximum. These improved flows after BMV appear to be secondary to reduction in LA pressure and improved cardiac output.

Supra-valvular aortic stenosis in a patient with homozygous familial hypercholesterolaemia

An 18-year-old female was referred for a cardiac murmur before surgical excision of large subcutaneous swellings over bi-lateral trochanteric areas ( Panel A ). On evaluation they were found to be tendon-xanthomas, that also involved the gluteal-folds, finger web-spaces ( Panel B ), and tendons of the foot. Corneal arcus was also noted ( Panel C ). Her total cholesterol of 696 mg% and low-density lipoprotein (LDL) cholesterol of 648 mg% were consistent with familial …

Acute myocardial infarction being the presentation of dengue myocarditis.

Dengue fever is one of the most common vector-borne viral infections in tropical countries. Myocarditis is an uncommon complication of severe dengue fever. Sometimes, dengue myocarditis masquerades as acute myocardial infarction. We report here a case of a 22-year-old female, who presented with acute chest pain five days after the onset of a febrile episode. Initially she was diagnosed as acute myocardial infarction depending on the biochemical and echocardiography evidence. However, later investigation confirmed she was suffering from myocarditis due to dengue fever, which mimicked acute myocardial infarction. A Medline search revealed only few other reported cases of dengue myocarditis that mimicked of acute myocardial infarction.

Anomalous Mitral Arcade Variant with Accessory Mitral Leaflet and Chordae Presenting for the First Time with Acute Decompensated Heart Failure in an Adult

The anomalous mitral arcade is a rare congenital malformation of the mitral valve and its tensor apparatus. It is characterized by enlarged papillary muscles connected to each other and to the free edge of the anterior mitral leaflet by a bridge of fibrous tissue. We report a rare variant of anomalous mitral arcade that was associated with accessory mitral leaflet in subaortic area and accessory chordae. Our patient was asymptomatic till the age of 18 years, when he presented for the first time in acute decompensated heart failure secondary to severe mitral regurgitation and left ventricular dysfunction. The patient had rapid deterioration with fatal outcome.

Incidence and Predictors of Atrial Septal Defect after Percutaneous Transvenous Mitral Commissurotomy – A Transesophageal Echocardiographic Study of 209 Cases

Background: The incidence of atrial septal defect (ASD) after percutaneous transvenous mitral commissurotomy (PTMC) ranges from 15.2% to 92% in small studies. Aim: To estimate the incidence of atrial septal defect (ASD) following PTMC and to determine the factors contributing to its development. Methods: We studied 209 patients with mitral stenosis (MS) undergoing PTMC. Transesophageal echocardiography (TEE) with color Doppler examination was performed to detect ASD. Results: TEE demonstrated ASD in 139 (66.5%) of 209 patients. The mean diameter of the interatrial septal defect detected by TEE was 4.47 ± 1.7 mm. The most common site of septal puncture was the inferior vena caval side of the interatrial septum followed by fossa ovalis. Color flow imaging across the defect showed left to right shunting in all the patients (100%). We examined the relationship of age, Wilkins score, left atrial volumes, the mitral valve orifice area, mitral valve gradient, and the degree of mitral and tricuspid regurgitation between the group that developed ASD and the group without ASD and found that none of these factors predicted the development of ASD. A residual ASD was seen in 11 patients (8.7%) at 6‐month follow‐up. Conclusion: Incidence of residual atrial septal defect immediately following PTMC by TEE color flow Doppler imaging is 66.5%. Surrogate markers of elevated left atrial pressures do not determine the development of atrial septal defect after PTMC. The majority of the defects close spontaneously and a residual defect is observed in 8.7% patients at 6 months.

An unusual case of complete atrioventricular block causing Takotsubo syndrome

Complete atrioventricular (AV) block in association with Takotsubo syndrome (TS) has been well recognized, but the cause and effect relationship has not been elucidated. We describe a 78-year-old female who presented with complete AV block but one week later developed new-onset, diffuse T-wave inversions, QT prolongation, and acceleration of junctional escape rate. Left ventriculogram revealed features typical of TS. One year after permanent pacemaker implantation, complete AV block persisted despite the reversal of wall motion defects implying that conduction abnormality was the trigger of TS rather than its consequence.

Idiopathic Dilatation of the Right Atrium: Clinical and Diagnostic Pitfalls – A Series of 3 Cases

Idiopathic dilatation of the right atrium (IDRA), also known as the giant right atrial aneurysm (RAA), is a rare anomaly, usually asymptomatic and of unknown etiology. It can be associated with atrial arrhythmias, severe tricuspid regurgitation (TR), congestive heart failure, thrombus formation leading to pulmonary embolism, paradoxical embolism, and stroke. IDRA can be misdiagnosed as Ebstein’s anomaly or Uhl’s anomaly due to the hugely dilated right atrium (RA) in both the anomalies. The imaging modalities such as two-dimensional transthoracic echocardiography (2DTTE), threedimensional (3DTTE), computed tomography (CT), and cardiac magnetic resonance imaging (MRI) can be very useful in differentiating the various causes for dilated RA and thereby aiding in the management of this congenital abnormality.

Response to the letter to the editor: Complete heart block and Takotsubo syndrome: Dissecting the pathophysiology

We reviewed the letter by John Madias [1] and would like to thank him for the constructive and encouraging remarks regarding our case report. Complete AV block occurring in association with Takotsubo syndrome (TS) has been an enigma, and the cause and effect relationship has not been elucidated. The occurrence of AV block in the context of exaggerated sympathetic activation seems paradoxical. However, we could document the chronological sequence of the occurrence of AV block and the subsequent TS in our patient [2]. As illustrated by our case report, most cases of complete AV block associated with TS that persist on long-term followup are probably the triggers of TS rather than its consequence. Nevertheless, transient AV blocks have also been reported in association with TS, but the pathophysiology of rhythm disturbance in such cases has not been elucidated. Whether AV blocks can occur as a consequence of TS is controversial. Life-threatening stressful stimuli are associated with a generalized autonomic storm, with early events dominated by sympathetic effects and later events by parasympathetic effects [3]. Quantifying sympathetic and parasympathetic activity serially from the time of presentation can provide valuable insights into the pathophysiology of this condition. As proposed by Madias, measuring thoracic skin sympathetic activity employing conventional ECG electrodes represents a novel noninvasive surrogate of stellate ganglion activity and the extent of cardiac sympathetic activation [4,5]. We hope that future studies of TS and AV block will incorporate careful assessment of autonomic function that can help in unraveling the association between the two conditions.

Coarctoplasty and Stenting in a Case of Ventricular Septal Defect With Eisenmenger’s Syndrome: A Clinical Dilemma

Coarctoplasty with stenting is often an effective strategy in cases of recoarctation following surgical repair. The potential benefit of coarctoplasty in a patient with Eisenmenger’s syndrome is unknown. We describe the case of a 21-year-old male who presented with claudication of lower limbs. He was known to have congenital heart disease, consisting of ventricular septal defect, patent ductus arteriosus (PDA), and coarctation of the aorta. Coarctation repair and PDA ligation had been done at two months of age. At the time of presentation for evaluation of claudication, echocardiography revealed severe coarctation and evidence of Eisenmenger’s syndrome. This patient subsequently underwent balloon angioplasty and stenting of coarctation without any increase in cyanosis.