Dual left anterior descending coronary artery
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This document describes 4 types of dual left anterior descending coronary artery anatomies. Type I involves a long parallel LAD and short LAD providing diagonals. Type II has the long LAD on the right ventricle and short LAD providing septals while the long provides diagonals. Type III has an intramyocardial long LAD course. Type IV has the long LAD originating anomalously from the right coronary artery before entering the anterior interventricular groove. A video is provided showing Type I dual LAD with a chronic total occlusion of the larger LAD.
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Transcatheter closure of patent ductus arteriosus (PDA) is feasible in low-birth-weight infants. A female baby was born prematurely with a birth weight of 924 g. She had a PDA measuring 3.7 mm. She was dependent on positive pressure ventilation for congestive heart failure in addition to the heart failure medications. She could not be discharged from the hospital even after 79 days of birth, and even though her weight reached 1.9 kg in the neonatal intensive care unit. We attempted to plug the PDA using an Amplatzer Piccolo Occluder, but the device failed to anchor. Then, the PDA was plugged using a 4-6 Amplatzer Duct Occluder using a 6-Fr sheath which was challenging.
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Accidental misplacement of the limb lead electrodes is a common cause of ECG abnormality and may simulate pathology such as ectopic atrial rhythm, chamber enlargement or myocardial ischaemia and infarction
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...
Device closure of an eccentric atrial septal defect can be challenging and needs technical modifications to avoid unnecessary complications. Here, we present a case of a 45-year-old woman who underwent device closure of an eccentric defect with a large device. The patient developed pericardial effusion and left-sided pleural effusion due to injury to the junction of right atrium and superior vena cava because of the malalignment of the delivery sheath and left atrial disc before the device was pulled across the eccentric defect despite releasing the left atrial disc in the left atrium in place of the left pulmonary vein. These two serious complications were managed conservatively with close monitoring of the case during and after the procedure.
Arrythmia-IV.pptx
1) Bradycardia can be caused by abnormalities in the conduction system or autonomic nervous system. The conduction system includes the sinus node, AV node, His-Purkinje system and different types of heart block can occur when impulses are blocked at different locations.
2) There are three main types of AV block - first degree, second degree (Mobitz types I and II), and third degree. High grade AV block involves blockage of two or more consecutive impulses.
3) Third degree or complete heart block results in complete dissociation between the atria and ventricles with independent pacemakers. It can occur at the AV node or below in the His-Purkin
Arrythmia-III.pptx
1. Bradycardia is defined as a resting heart rate below 50 beats per minute. It can be physiological or pathological.
2. Sinus bradycardia originates from the sinus node and has a normal P wave morphology with a prolonged PR interval. It can be caused by increased vagal tone, medications, or hypothyroidism.
3. Sick sinus syndrome is characterized by sinus bradycardia, sinus arrest, or combinations of sinus node and AV node dysfunction. It may involve intermittent bradycardia and tachycardia. Pacemaker implantation is usually treatment.
Arrythmia-II.pptx
This document discusses ventricular arrhythmias including their origins, characteristics, classifications, and causes. It provides details on:
- The sites of origin for supraventricular tachycardia (SVT) and ventricular arrhythmias.
- Characteristics that distinguish SVT from ventricular arrhythmias such as QRS width.
- Classifications of ventricular arrhythmias including premature ventricular complexes, ventricular tachycardia, fibrillation, and electrical storm.
- Causes and characteristics of different types of ventricular tachycardia such as monomorphic VT, polymorphic VT, and torsades de pointes.
- Investigations and treatments for ventricular arrhythmias including cardiac imaging
Arrythmia-I.pptx
This document provides information on supraventricular tachycardia (SVT), including:
- The anatomy and conduction system of the heart that is relevant to SVT.
- The mechanisms that can cause cardiac arrhythmias, including disorders of impulse formation, conduction, and combinations of the two.
- Characteristics used to classify different types of arrhythmias based on rate, rhythm, site of origin, and QRS morphology.
- Specific types of SVT like atrial fibrillation, AV nodal reentry tachycardia, and accessory pathway mediated tachycardias.
- Methods for diagnosing and treating SVT such as electrophysiology studies, catheter ablation
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...
A 57-year-old male presented with recurrent palpitations. He was diagnosed with rheumatic mitral stenosis, right posterior septal accessory pathway and atrial flutter. An electrophysiological study after percutaneous balloon mitral valvotomy showed that the palpitations were due to atrial flutter with right bundle branch aberrancy. The right posterior septal pathway was a bystander because it had a higher refractory period than the atrioventricular node.
Anticoagulation therapy during pregnancy
This document discusses anticoagulation therapy options during pregnancy for different cardiac conditions. It notes that vitamin K antagonists (VKAs) should be avoided in the first trimester due to risk of embryopathy but can be used in the second and third trimester with risks of 0.7-2% of foetopathy. Unfractionated heparin does not cross the placenta but its use throughout pregnancy is not recommended due to risk of foetopathy. Low molecular weight heparin is considered the safest option for anticoagulation in weeks 6-12 when risk of embryopathy is a concern and has not been associated with risk of foetopathy. Fondaparinux use should be limited
Coronary guidewire
Percutaneous balloon dilatation, first described by
Andreas Gruentzig in 1979, was initially performed
without the use of guidewires.1 The prototype
balloon catheter was developed as a double lumen
catheter (one lumen for pressure monitoring or
distal perfusion, the other lumen for balloon inflation/deflation) with a short fixed and atraumatic
guidewire at the tip. Indeed, initially the technique
involved advancing a rather rigid balloon catheter
freely without much torque control into a coronary
artery. Bends, tortuosities, angulations, bifurcations,
and eccentric lesions could hardly, if at all, be negotiated, resulting in a rather frustrating low procedural success rate whenever the initial limited
indications (proximal, short, concentric, noncalcified) were negated.2 Luck was almost as
important as expertise, not only for the operator,
but also for the patient. It is to the merit of
Simpson who, in 1982, introduced the novelty of
advancing the balloon catheter over a removable
guidewire, which had first been advanced in the
target vessel.3 This major technical improvement
resulted overnight in a notable increase in the procedural success rate. Guidewires have since evolved
into very sophisticated devices.
Intracoronary optical coherence tomography
Optical coherence tomography-guided algorithm for percutaneous coronary intervention. Vessel diameter should be assessed using the external elastic lamina (EEL)-EEL diameter at the reference segments, and rounded down to select interventional devices (balloons, stents). If the EEL cannot be identified, luminal measures are used and rounded up to 0.5 mm larger for selection of the devices. Optical coherence tomography (OCT)-guided optimisation strategies post stent implantation per EEL-based diameter measurement and per lumen-based diameter measurement are shown. For instance, if the distal EEL-EEL diameter measures 3.2 mm×3.1 mm (i.e., the mean EEL-based diameter is 3.15 mm), this number is rounded down to the next available stent size and post-dilation balloon to be used at the distal segment. Thus, a 3.0 mm stent and non-compliant balloon diameter is selected. If the proximal EEL cannot be visualised, the mean lumen diameter should be used for device sizing. For instance, if the mean proximal lumen diameter measures 3.4 mm, this number is rounded up to the next available balloon diameter (within up to 0.5 mm larger) for post-dilation. MLA: minimal lumen area; MSA: minimal stent area;NC: non-compliant
Brugada syndrome
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
A roadmap for the human development
The Human Developmental Cell Atlas (HDCA) initiative, which is part of the Human Cell Atlas, aims to create a comprehensive reference map of cells during development. This will be critical to understanding normal organogenesis, the effect of mutations, environmental factors and infectious agents on human development, congenital and childhood disorders, and the cellular basis of ageing, cancer and regenerative medicine. Here we outline the HDCA initiative and the challenges of mapping and modelling human development using state-of-the-art technologies to create a reference atlas across gestation. Similar to the Human Genome Project, the HDCA will integrate the output from a growing community of scientists who are mapping human development into a unified atlas. We describe the early milestones that have been achieved and the use of human stem-cell-derived cultures, organoids and animal models to inform the HDCA, especially for prenatal tissues that are hard to acquire. Finally, we provide a roadmap towards a complete atlas of human development.
Intra aortic balloon pump
The treatment of patients with advanced acute heart failure is still challenging.
Intra-aortic balloon pump (IABP) has widely been used in the management of
patients with cardiogenic shock. However, according to international guidelines, its
routinary use in patients with cardiogenic shock is not recommended. This recommendation is derived from the results of the IABP-SHOCK II trial, which demonstrated
that IABP does not reduce all-cause mortality in patients with acute myocardial infarction and cardiogenic shock. The present position paper, released by the Italian
Association of Hospital Cardiologists, reviews the available data derived from clinical
studies. It also provides practical recommendations for the optimal use of IABP in
the treatment of cardiogenic shock and advanced acute heart failure.
Left ventricular false tendons
Left ventricular false tendons (LVFTs) are fibromuscular
structures, connecting the left ventricular
free wall or papillary muscle and the ventricular
septum.
There is some discussion about safety issues during
intense exercise in athletes with LVFTs, as these
bands have been associated with ventricular arrhythmias
and abnormal cardiac remodelling. However,
presence of LVFTs appears to be much more common
than previously noted as imaging techniques
have improved and the association between LVFTs
and abnormal remodelling could very well be explained
by better visibility in a dilated left ventricular
lumen.
Although LVFTsmay result in electrocardiographic abnormalities
and could form a substrate for ventricular
arrhythmias, it should be considered as a normal
anatomic variant. Persons with LVFTs do not appear
to have increased risk for ventricular arrhythmias or
sudden cardiac death.
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