Varun S. Narain

Post-traumatic left ventricular pseudoaneurysm

Left ventricular pseudoaneurysms (LVPs) occur as a complication of myocardial infarction, cardiac surgery and, rarely, due to thoracic trauma, infective pericarditis or iatrogenisis due to accidental perforation of the myocardium. Ventricular pseudoaneurysms are acquired by blood-filled spaces outside the cardiac chambers communicating with the ventricle. We present a case of LVP presented after a blunt non-penetrating chest injury. The patient underwent successful aneurysmorrhaphy.

Effect of Ivabradine on Heart Rate and Duration of Exercise in Patients With Mild-to-Moderate Mitral Stenosis: A Randomized Comparison With Metoprolol.

Background: Symptoms in mitral stenosis (MS) are heart rate (HR) dependent. Increase in HR reduces diastolic filling period with rise in transmitral gradient. By reducing HR, beta-blockers improve hemodynamics and relieve symptoms, but the use may be limited by side effects. The present randomized crossover study looked at comparative efficacy of ivabradine and metoprolol on symptoms, hemodynamics, and exercise parameters in patients with mild-to-moderate MS (mitral valve area, 1–2 cm2) in normal sinus rhythm. Material and Methods: Baseline clinical assessment, treadmill stress testing, and an echocardiographic Doppler evaluation were performed to determine resting HR, total exercise duration, mean gradient across mitral valve, and mean pulmonary artery systolic pressure (PASP). Patients were then allocated to either metoprolol or ivabradine to maximal tolerated doses over 6 weeks (metoprolol: 100 mg twice a day, ivabradine: 10 mg twice a day). Reevaluation was done at the end of this period, and all drugs stopped for washout over 2 weeks. Thereafter, the 2 groups were crossed over to the other drug that was continued for another 6 weeks. Assessment was again performed at the end of this period. Results: Thirty-three patients of 34 completed the protocol. Fifteen were male, mean age was 28.9 ± 6.6 years, all were in New York Heart Association class 2, and mean resting HR was 103.5 ± 7.2/min. Mean mitral valve area was 1.56 ± 0.16 cm2, mean PASP was 38.1 ± 5.1 mm Hg, and mean gradient across mitral valve was 10.6 ± 1.6 mm Hg. Significant decrease in baseline and peak exercise HR was observed at the end of follow-up with both drugs. Reduction in mitral valve gradient after ivabradine (42%) and metoprolol (37%) and reduction in PASP after both ivabradine (23%) and metoprolol (27%) were to a similar extent. Significant reduction in total exercise duration after both ivabradine and metoprolol therapy was observed. One patient developed blurring of vision with ivabradine therapy but did not require discontinuation of drug. An improvement in dyspnea of one grade was observed in all the patients by treatment with both ivabradine and metoprolol. Conclusions: Both metoprolol and ivabradine reduced symptoms and improved hemodynamics significantly from baseline to a similar extent. Ivabradine thus can be used effectively and safely in patients with MS in normal sinus rhythm who are intolerant or contraindicated for beta-blocker therapy.

Optimal fluid amount for haemodynamic benefit in cardiac tamponade.

Objectives: The present study was undertaken to assess the effect of volume expansion on cardiac haemodynamics in patients with cardiac tamponade and to ascertain an optimum amount of fluid that can produce the maximum benefit in tamponade patients. Background: In patients of tamponade, interim measures may occasionally be needed when facilities for pericardial fluid drainage are not immediately available. Intravascular volume expansion is the most commonly advocated measure but with limited scientific data. Methods: Patients ≥16 years of age with large circumferential pericardial effusion and showing echocardiographic evidence of cardiac tamponade were included. Haemodynamically unstable patients, those with structural heart diseases, pregnant females, and those undergoing haemodialysis were excluded. The various haemodynamic parameters were measured using Edwards Life Sciences Vigilance II monitor, Swan Ganz CCO catheter, intrapericardial access, and arterial access at baseline and after each 250 ml fluid over 5 min (total 1000 ml in 20 min). The entire fluid was drained at the end of the procedure. Results: A total of 28 patients constituted the study group, all of whom exhibited an improvement in haemodynamic parameters (systolic blood pressure, cardiac output) and a rise of the intracardiac pressures with volume expansion. Significant (p<0.05 ) increase in systolic and diastolic blood pressure, cardiac output, and cardiac index occurred up to 250–500 ml bracket; above which the significance was lost. A higher resting heart rate, a lower SBP at presentation, a higher initial intrapericardial pressure, and a lower cardiac index were the statistically significant predictors of a >15% increase in cardiac index. Conclusions: Rapid infusion of as little as 250 ml intravenous normal saline may improve the cardiac haemodynamics in a significant proportion of tamponade patients.

Symptomatic complete heart block leading to a diagnosis of Kearns–Sayre syndrome

Kearns-Sayre syndrome (KSS) is a rare syndrome characterized by the triad of progressive external ophthalmoplegia, pigmentary retinopathy and cardiac conduction system disturbances; it is a mitochondrial encephalomyopathy with which usually presents before the patient reaches the age of 20. Here we present a case report of a patient with KSS who presented with symptomatic complete heart block.

Effects of Digoxin in high risk chronic heart failure patients in the DIG trial: a pre specified subgroup analysis

Background: Despite a class IIa indication for Digoxin use in heart failure by both ACC/AHA and ESC, its use has been going down in the last decade. One of the reasons has been the result of The Digitalis Investigation Group (DIG) Trial. This randomized controlled study in 6800 patients of ambulatory heart failure (age ≥21 yrs, LV ejection fraction ≤45%, normal sinus rhythm) failed to show a mortality benefit from Digoxin use. It did however demonstrate a reduction in hospitalizations overall and for worsening heart failure. n nObjectives: Since more than half of these heart failure patients had high risk features characterized by class III–IV symptoms, or ejection fraction lower than 25% or with a CT ratio more than 55% a subanalysis of DIG Trial data was planned to see the effect of Digoxin in this subcategory in terms of the composite endpoints of mortality or hospitalizations over 2 years. n nPatients and methods: From the dataset of DIG patients obtained from the National Heart Blood and Lung Institute, 4367 high risk patients (mean age 64 years, 26% females) were analyzed. There were 2223 (51%) with class III–IV symptoms, 2256 (52%) with LVEF 55%. All high risk feature groups were analyzed separately and also together. n nPearson chi square and Wicoxon rank sum tests showed no significant difference in the baseline characteristics, including medical history, cause of heart failure and drug use between the three groups (except that dyspnea was more in the those with class II–IV symptoms). Outcomes were assessed using Kaplan Meier and Cox proportional hazard analyses. Statistical analysis was two tailed in all cases and a p value of <0.05 was considered significant. n nResults: Results at 24 months showed that all-cause mortality or all-cause hospitalization was significantly better with Digoxin use versus placebo. Hazard ratio for NYHA class III–IV was 0.88 (pxa0=xa00.012); 0.84 (pxa0=xa00.001) for LVEF 55%, absolute risk reduction being −2%, −6% and −4% respectively. There was an absolute risk reduction of −3% in favor of Digoxin if any of the three high risk feature was present (pxa0≤xa00.001). Also, significantly less patients receiving Digoxin experienced heart failure related mortality or hospitalization. HR was 0.65 (pxa0 55%(absolute risk reduction ofxa0−11%, −12%, −11%, −10% respectively and −11% when any of the high risk features were present; pxa0=xa00.001). n nConclusion: Digoxin use reduced the primary endpoint of all-cause and heart failure mortality or hospitalizations in high risk heart failure patients. This effect was primarily driven by reduction in hospitalizations with no significant effect on mortality.