Objective To evaluate the presentation, management, and outcomes of patients hospitalized for heart failure (HF) in Trivandrum, India. Methods The Trivandrum Heart Failure Registry (THFR) enrolled consecutive admissions from 13 urban and five rural hospitals in Trivandrum with a primary diagnosis of HF from January to December 2013. Clinical characteristics at presentation, treatment, in‐hospital outcomes, and 90‐day mortality data were collected. ‘Guideline‐based’ medical treatment was defined as the combination of beta‐blockers, angiotensin‐converting enzyme inhibitors or angiotensin receptor blockers, and aldosterone receptor blockers in patients with left ventricular systolic dysfunction (LVSD). Results We enrolled 1205 cases (834 men, 69%) into the registry. Mean (standard deviation) age was 61.2 (13.7) years. The most common HF aetiology was ischaemic heart disease (IHD) (72%). Heart failure with preserved ejection fraction (≥45%) constituted 26% of the population. The median hospital stay was 6 days (interquartile range = 4–9 days) with an in‐hospital mortality rate of 8.5% (95% confidence interval 6.9–10.0). The 90‐day all‐cause mortality rate was 2.43 deaths per 1000 person‐days (95% confidence interval 2.11–2.78). Guideline‐based medical treatment was given to 19% and 25% of patients with LVSD during hospital admission and at discharge, respectively. Older age, lower education, poor ejection fraction, higher serum creatinine, New York Heart Association functional class IV, and suboptimal medical treatment were associated with higher risk of 90‐day mortality. Conclusion Patients hospitalized with HF in the THFR were younger, more likely to be men, had a higher prevalence of IHD, reported longer length of hospital stay, and higher mortality compared with published data from other registries. We also identified key areas for improving hospital‐based HF medical care in Trivandrum.
BackgroundEndocardial mapping for scars and abnormal electrograms forms the most essential component of ventricular tachycardia ablation. The utility of ultra‐high resolution mapping of ventricular scar was assessed using a multielectrode contact mapping system in a chronic canine infarct model.MethodsChronic infarcts were created in five anesthetized dogs by ligating the left anterior descending coronary artery. Late gadolinium‐enhanced magnetic resonance imaging (LGE MRI) was obtained 4.9 ± 0.9 months after infarction, with three‐dimensional (3D) gadolinium enhancement signal intensity maps at 1‐mm and 5‐mm depths from the endocardium. Ultra‐high resolution electroanatomical maps were created using a novel mapping system (Rhythmia Mapping System, Rhythmia Medical/Boston Scientific, Marlborough, MA, USA) Rhythmia Medical, Boston Scientific, Marlborough, MA, USA with an 8.5F catheter with mini‐basket electrode array (64 tiny electrodes, 2.5‐mm spacing, center‐to‐center).ResultsThe maps contained 7,754 ± 1,960 electrograms per animal with a mean resolution of 2.8 ± 0.6 mm. Low bipolar voltage (<2 mV) correlated closely with scar on the LGE MRI and the 3D signal intensity map (1‐mm depth). The scar areas between the MRI signal intensity map and electroanatomic map matched at 87.7% of sites. Bipolar and unipolar voltages, compared in 592 electrograms from four MRI‐defined scar types (endocardial scar, epicardial scar, mottled transmural scar, and dense transmural scar) as well as normal tissue, were significantly different. A unipolar voltage of <13 mV correlated with transmural extension of scar in MRI. Electrograms exhibiting isolated late potentials (ILPs) were manually annotated and ILP maps were created showing ILP location and timing. ILPs were identified in 203 ± 159 electrograms per dog (within low‐voltage areas) and ILP maps showed gradation in timing of ILPs at different locations in the scar.ConclusionsUltra‐high resolution contact electroanatomical mapping accurately localizes ventricular scar and abnormal myocardial tissue in this chronic canine infarct model. The high fidelity electrograms provided clear identification of the very low amplitude ILPs within the scar tissue and has the potential to quickly identify targets for ablation.
PurposeIron deposition has been shown to occur following myocardial infarction (MI). We investigated whether such focal iron deposition within chronic MI lead to electrical anomalies.MethodsTwo groups of dogs (ex-vivo (n = 12) and in-vivo (n = 10)) were studied at 16 weeks post MI. Hearts of animals from ex-vivo group were explanted and sectioned into infarcted and non-infarcted segments. Impedance spectroscopy was used to derive electrical permittivity () and conductivity (). Mass spectrometry was used to classify and characterize tissue sections with (IRON+) and without (IRON-) iron. Animals from in-vivo group underwent cardiac magnetic resonance imaging (CMR) for estimation of scar volume (late-gadolinium enhancement, LGE) and iron deposition (T2*) relative to left-ventricular volume. 24-hour electrocardiogram recordings were obtained and used to examine Heart Rate (HR), QT interval (QT), QT corrected for HR (QTc) and QTc dispersion (QTcd). In a fraction of these animals (n = 5), ultra-high resolution electroanatomical mapping (EAM) was performed, co-registered with LGE and T2* CMR and were used to characterize the spatial locations of isolated late potentials (ILPs).ResultsCompared to IRON- sections, IRON+ sections had higher, but no difference in. A linear relationship was found between iron content and (p<0.001), but not (p = 0.34). Among two groups of animals (Iron (<1.5%) and Iron (>1.5%)) with similar scar volumes (7.28%±1.02% (Iron (<1.5%)) vs 8.35%±2.98% (Iron (>1.5%)), p = 0.51) but markedly different iron volumes (1.12%±0.64% (Iron (<1.5%)) vs 2.47%±0.64% (Iron (>1.5%)), p = 0.02), QT and QTc were elevated and QTcd was decreased in the group with the higher iron volume during the day, night and 24-hour period (p<0.05). EAMs co-registered with CMR images showed a greater tendency for ILPs to emerge from scar regions with iron versus without iron.ConclusionThe electrical behavior of infarcted hearts with iron appears to be different from those without iron. Iron within infarcted zones may evolve as an arrhythmogenic substrate in the post MI period.
Both Accura and Inoue balloon mitral valvotomy balloons are effective in providing relief from hemodynamically significant mitral stenosis in terms of gain in valve area and reduction in trans mitral gradient. Both groups have similar procedural success and complication rates, restenosis, and follow-up events at 1 year. Both balloons could be reused multiple times and Accura balloon is found to be more cost effective.
Pulmonary artery pressure (PAP) is known to regress after successful balloon mitral valvotomy (BMV). Data of persistent pulmonary artery hypertension (PPAH) following BMV is scarce. We analyzed the clinical, echocardiographic, and hemodynamic data of 701 consecutive patients who have undergone successful BMV in our institute from 1997 to 2003. Data of 287 patients who had PPAH (defined by pulmonary artery systolic pressure [PASP] of ≥ 40 mmHg at one year following BMV) were compared to the data of 414 patients who did not have PPAH. Patients who had PPAH were older (39.9 ± 9.9 years vs. 29.4 ± 10.1; P < 0.001). They had higher prevalence of atrial fibrillation (AF; 21.9 vs. 12.1%, P < 0.05), moderate or severe pulmonary artery hypertension (PAH) defined as PASP more than 50 mmHg (43.5 vs. 33.8%, P = 0.00), anatomically advanced mitral valve disease as assessed by Wilkin's echocardiographic score > 8 (33.7 vs. 23.2%, P < 0.001), and coexistent aortic valve disease (45.6 vs. 37.9%, P < 0.001) at the baseline. Those patients with PPAH had comparatively lower immediate postprocedural mitral valve area (MVA). On follow-up of more than five years, the occurrence of restenosis (39.3 vs. 10.1%, P = 0.000), new onset heart failure (14% vs. 4%, P < 0.05) and need for reinterventions (9.5% vs. 2.8%, P < 0.05) were higher in the PPAH group. Patients with PPAH were older, sicker, and had advanced rheumatic mitral valve disease. They had higher incidence of restenosis, new onset heart failure, and need for reinterventions on long term follow-up. PPAH represents an advanced stage of rheumatic valve disease and indicates chronicity of the disease, which may be the reason for the poorer prognosis of these patients. Patients with PPAH requires intense and more frequent follow-up.
AV node reentry, catheter ablation, retrograde conduction, Wenkebach blockA 45-year-old woman was referred for radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead electrocardiography (ECG) was normal during sinus rhythm. She was taking calcium channel blockers and that was stopped 5 half-lives prior to the procedure. The electrophysiological study showed a normal atrio-Hisian (AH) interval of 104 milliseconds and His-ventricular (HV) interval of 42 milliseconds during sinus rhythm. Retrograde conduction was central and decremental. Anterograde study demonstrated dual atrioventricular (AV) nodal physiology. Atrial pacing protocols easily and reproducibly induced narrow QRS tachycardia. What is the mechanism? CommentaryThe tachycardia represents a slightly irregular supraventricular tachycardia without the requirement for the atrium, ruling out atrial tachycardia and atrioventricular reentry. This leaves only junctional tachycardia (JT), AV nodal reentry, and the much less commonly observed nodoventricular reentry. JT is unlikely by the method of induction and the slight irregularity. The third and seventh cycles of the tachycardia showed prolongation of RR interval as shown in Figures 1 and 2. The intracardiac recordings (Fig. 2) showed 3:2 ventriculoatrial (VA) response for the first 3 beats followed by 4:3 VA response and 3:2 VA response for the last 3 beats. A retrograde VA Wenkebach pattern is noted as evidenced by the progressive prolongation of the VA interval till it stops conducting to atrium. The atrial activation J Cardiovasc Electrophysiol, Vol. 00, pp. 1-2, xxxx 2016. Figure 2. The AH and the His-His (HH) intervals are essentially constant except for the cycle following the retrograde block, during which they are significantly prolonged. Retrograde conduction to atrium resumes after the prolonged AH and HH intervals and it is followed by retrograde HA Wenkebach.The tachycardia represents slow-slow type of AV nodal reentrant tachycardia with retrograde HA Wenkebach and abrupt prolongation of the anterograde AV nodal conduction time after the HA block, as evidenced by the increase in the HH interval, with subsequent resumption of retrograde HA conduction. Prolongation of the anterograde conduction time allowed restoration of retrograde conduction of the subsequent beat, suggesting a dependency and relationship of retrograde conduction on the anterograde AV nodal conduction time by an undefined mechanism. The underlying morphological substrate behind this phenomenon involves 2 anatomical or functional AV nodal or intranodal circuits in the anterograde limb with distinct conduction properties, which is manifested after the retrograde block and a slow conducting AV nodal circuit as the retrograde limb.The patient has undergone a successful slow pathway ablation and neither dual AV node physiology nor tachycardia could be demonstrated after that.
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