Management of Hypertension
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Usually hypertension is defined as blood pressure above 140/90, and is considered severe if the pressure is above 180/120. High blood pressure often has no symptoms. Over time, if untreated, it can cause health conditions, such as heart disease and stroke. Eating a healthier diet with less salt, exercising regularly and taking medication can help lower blood pressure
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Willens's syndrome.pptx
Wellens syndrome. Wellens syndrome (also referred to as LAD coronary T-wave syndrome) refers to an ECG pattern specific for critical stenosis of the proximal left anterior descending artery. The anomalies described occur in patients with recent anginal chest pain, and do not have chest pain when the ECG is recorded.
Intensive care of congenital heart disease.pptx
Congenital defects can put a strain on the heart, causing it to work harder. To stop your heart from getting weaker with this extra work, your doctor may try to treat you with medications. They are aimed at easing the burden on the heart muscle. You need to control your blood pressure if you have any type of heart problem.
Management of Hypetension.pptx
Changing your lifestyle can help control and manage high blood pressure. Your health care provider may recommend that you make lifestyle changes including:
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight
Limiting alcohol
Not smoking
Getting 7 to 9 hours of sleep daily
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CRISPR technologies have progressed by leaps and bounds over the past decade, not only having a transformative effect on
biomedical research but also yielding new therapies that are poised to enter the clinic. In this review, I give an overview of (i)
the various CRISPR DNA-editing technologies, including standard nuclease gene editing, base editing, prime editing, and epigenome editing, (ii) their impact on cardiovascular basic science research, including animal models, human pluripotent stem
cell models, and functional screens, and (iii) emerging therapeutic applications for patients with cardiovascular diseases, focusing on the examples of Hypercholesterolemia, transthyretin amyloidosis, and Duchenne muscular dystrophy.
Pacemaker Pocket Infection After Splenectomy
A post-splenectomy patient suffers from frequent infections due to capsulated bacteria like Streptococcus
pneumoniae, Hemophilus influenzae, and Neisseria meningitidis despite vaccination because of a lack of
memory B lymphocytes. Pacemaker implantation after splenectomy is less common. Our patient underwent
splenectomy for splenic rupture after a road traffic accident. He developed a complete heart block after
seven years, during which a dual-chamber pacemaker was implanted. However, he was operated on seven
times to treat the complication related to that pacemaker over a period of one year because of various
reasons, which have been shared in this case report. The clinical translation of this interesting observation
is that, though the pacemaker implantation procedure is a well-established procedure, the procedural
outcome is influenced by patient factors like the absence of a spleen, procedural factors like septic measures,
and device factors like the reuse of an already-used pacemaker or leads.
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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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Congenital defects can put a strain on the heart, causing it to work harder. To stop your heart from getting weaker with this extra work, your doctor may try to treat you with medications. They are aimed at easing the burden on the heart muscle. You need to control your blood pressure if you have any type of heart problem.
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Changing your lifestyle can help control and manage high blood pressure. Your health care provider may recommend that you make lifestyle changes including:
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight
Limiting alcohol
Not smoking
Getting 7 to 9 hours of sleep daily
CRISPR and cardiovascular diseases.pdf
CRISPR technologies have progressed by leaps and bounds over the past decade, not only having a transformative effect on
biomedical research but also yielding new therapies that are poised to enter the clinic. In this review, I give an overview of (i)
the various CRISPR DNA-editing technologies, including standard nuclease gene editing, base editing, prime editing, and epigenome editing, (ii) their impact on cardiovascular basic science research, including animal models, human pluripotent stem
cell models, and functional screens, and (iii) emerging therapeutic applications for patients with cardiovascular diseases, focusing on the examples of Hypercholesterolemia, transthyretin amyloidosis, and Duchenne muscular dystrophy.
Pacemaker Pocket Infection After Splenectomy
A post-splenectomy patient suffers from frequent infections due to capsulated bacteria like Streptococcus
pneumoniae, Hemophilus influenzae, and Neisseria meningitidis despite vaccination because of a lack of
memory B lymphocytes. Pacemaker implantation after splenectomy is less common. Our patient underwent
splenectomy for splenic rupture after a road traffic accident. He developed a complete heart block after
seven years, during which a dual-chamber pacemaker was implanted. However, he was operated on seven
times to treat the complication related to that pacemaker over a period of one year because of various
reasons, which have been shared in this case report. The clinical translation of this interesting observation
is that, though the pacemaker implantation procedure is a well-established procedure, the procedural
outcome is influenced by patient factors like the absence of a spleen, procedural factors like septic measures,
and device factors like the reuse of an already-used pacemaker or leads.
Piccolo Duct Occluder.pdf
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.
MISPLACED ECG LEADS.pptx
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.
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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.
Approach to medina 001 bifurcations
The optimal management of bifurcation lesions has received significant interest in recent years and remains a matter of debate among the
interventional cardiology community. Bifurcation lesions are encountered in approximately 21% of percutaneous coronary intervention procedures
and are associated with an increased risk of major adverse cardiac events. The Medina classification has been developed in an attempt to
standardise the terminology when describing bifurcation lesions. The focus of this article is on the management of the Medina 0,0,1 lesion
(‘Medina 001’), an uncommon lesion encountered in <5% of all bifurcations. Technical considerations, management options and interventional
techniques relating to the Medina 001 lesion are discussed. In addition, current published data supporting the various proposed interventional
treatment strategies are examined in an attempt to delineate an evidence-based approach to this uncommon lesion.
Heparin resistance
Drug resistance is defined as the lack of expected response to a standard therapeutic dose of a drug or as resistance resulting from biologic changes in the target, as occurs in antibiotic resistance. Heparin resistance, the failure to achieve a specified anticoagulation level despite the use of what is considered to be an adequate dose of heparin, is neither well understood nor well defined. Heparin resistance usually refers to an effect of unfractionated heparin, for which doses are measured and adjusted, rather than low-molecular-weight heparin, which is not routinely monitored with laboratory testing. Although it is infrequently invoked in inpatient settings, heparin resistance has been reported in critically ill patients with coronavirus disease 2019 (Covid-19) who are at high risk for thrombosis.1-3 This review provides a clinical summary of heparin resistance and potential management strategies.
Surgical repair of patent ductus arteriosus history timeline
Congenital cardiac surgery is one of the most challenging and fascinating branches of modern medicine which continues to
advance in areas and improving outcomes, post-operative and pre-operative care.
Patent Ductus Arteriosus was the first congenital heart lesion to be successfully corrected surgically. The landmark surgery was
performed by Dr. Robert E. Gross in 1938 and opened up the possibility of subsequent surgical correction of various other lesions,
which were considered to be untreatable previously. The first successful surgical closure of persistent ductus arteriosus (PDA)
was preceded by years of work and contributed by various surgeons, physicians, and anatomists, dating all the way back to
the 1st century. They are all worthy of recognition and praise.
This article covers the important events related to PDA lesions including its first identification, followed by its description
in various texts and sources over the course of time, failed attempts at surgical correction, and disputes regarding credits.
These contributions to the branch cannot be overstated and serves as an inspiration to cardiac surgeons all over the world
and to students, interns, and newly graduated doctors as well, who would one day like to be part of this fascinating branch.
The function of the thymus
Origin and migration of T and B cells. Hemopoietic stem cells originating in the yolk sac, fetal liver, or bone
marrow migrate through the blood to the thymus, where they differentiate into T lymphocytes. Others
differentiate within the bone marrow in mammals, or the bursa of Fabricius in birds, to produce B cells.
Mature T and B cells circulate in the blood and lymph and colonize the T and B cell compartments
of the lymphoid tissues
Management of premature ventricular complexes
Isolated monomorphic premature ventricular complexes (PVCs) without
structural heart disease are generally benign.
► Frequent PVCs can cause reversible cardiomyopathy or aggravate an existing
cardiomyopathy.
► Short coupled PVCs can trigger sustained ventricular fibrillation. These are
often from the Purkinje tissue or rarely the outflow tract.
► Beta blockers are considered first-line therapy but have low efficacy.
Catheter ablation and AADs are reasonable to suppress PVCs in appropriate
patients.
► Ablation is often curative and success depends on location and accessibility
of PVCs.
► Implantable defibrillators are reasonable in patients at higher risk of sudden
cardiac death.
Hemodynamics for the heart failure
This article reviews the role of invasive hemodynamics in the care of patients across the
entire spectrum of human heart failure.
Conceptual principles of ventricular function, ventricular-arterial interaction, load
response, and ventricular interaction in the right and left heart are reviewed.
Principles and practice of invasive exercise testing are provided, along with detailed
discussions on the role of invasive hemodynamics in the evaluation and management of
advanced heart failure, shock, mechanical circulatory support, and pulmonary
hypertension.
Bifurcation stenting
Significant unprotected left main (LM) coronary artery disease is present in <10% of patients undergoing coronary angiography. In autopsy research, a mean LM length of 10.8 mm ± 5.2 mm (range 2–23 mm), mean LM diameter 4.9 mm ± 0.8 mm and mean angle between the left anterior descending (LAD) and left circumflex (LCx) of 86.7° ± 28.8° has been described. This angle value positively correlated with LM length.2 Further studies showed that long LM developed stenoses more frequently near the distal bifurcation compared to near the ostium (77% versus 18%).7 It is also worth emphasising that LM bifurcation disease is rarely focal and that both sides of the carina are almost never disease-free. Furthermore, continuous plaque from the LM into the proximal LAD artery has been reported in 90% of cases.8 Summarised below are the most crucial LM peculiarities (in comparison with non-LM bifurcations), which should be taken into consideration when distal LM stenosis PCI is planned:
Valve in-valve implantation into a failed mechanical prosthetic aortic valve
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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.
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.
Approach to medina 001 bifurcations
The optimal management of bifurcation lesions has received significant interest in recent years and remains a matter of debate among the
interventional cardiology community. Bifurcation lesions are encountered in approximately 21% of percutaneous coronary intervention procedures
and are associated with an increased risk of major adverse cardiac events. The Medina classification has been developed in an attempt to
standardise the terminology when describing bifurcation lesions. The focus of this article is on the management of the Medina 0,0,1 lesion
(‘Medina 001’), an uncommon lesion encountered in <5% of all bifurcations. Technical considerations, management options and interventional
techniques relating to the Medina 001 lesion are discussed. In addition, current published data supporting the various proposed interventional
treatment strategies are examined in an attempt to delineate an evidence-based approach to this uncommon lesion.
Heparin resistance
Drug resistance is defined as the lack of expected response to a standard therapeutic dose of a drug or as resistance resulting from biologic changes in the target, as occurs in antibiotic resistance. Heparin resistance, the failure to achieve a specified anticoagulation level despite the use of what is considered to be an adequate dose of heparin, is neither well understood nor well defined. Heparin resistance usually refers to an effect of unfractionated heparin, for which doses are measured and adjusted, rather than low-molecular-weight heparin, which is not routinely monitored with laboratory testing. Although it is infrequently invoked in inpatient settings, heparin resistance has been reported in critically ill patients with coronavirus disease 2019 (Covid-19) who are at high risk for thrombosis.1-3 This review provides a clinical summary of heparin resistance and potential management strategies.
Surgical repair of patent ductus arteriosus history timeline
Congenital cardiac surgery is one of the most challenging and fascinating branches of modern medicine which continues to
advance in areas and improving outcomes, post-operative and pre-operative care.
Patent Ductus Arteriosus was the first congenital heart lesion to be successfully corrected surgically. The landmark surgery was
performed by Dr. Robert E. Gross in 1938 and opened up the possibility of subsequent surgical correction of various other lesions,
which were considered to be untreatable previously. The first successful surgical closure of persistent ductus arteriosus (PDA)
was preceded by years of work and contributed by various surgeons, physicians, and anatomists, dating all the way back to
the 1st century. They are all worthy of recognition and praise.
This article covers the important events related to PDA lesions including its first identification, followed by its description
in various texts and sources over the course of time, failed attempts at surgical correction, and disputes regarding credits.
These contributions to the branch cannot be overstated and serves as an inspiration to cardiac surgeons all over the world
and to students, interns, and newly graduated doctors as well, who would one day like to be part of this fascinating branch.
The function of the thymus
Origin and migration of T and B cells. Hemopoietic stem cells originating in the yolk sac, fetal liver, or bone
marrow migrate through the blood to the thymus, where they differentiate into T lymphocytes. Others
differentiate within the bone marrow in mammals, or the bursa of Fabricius in birds, to produce B cells.
Mature T and B cells circulate in the blood and lymph and colonize the T and B cell compartments
of the lymphoid tissues
Management of premature ventricular complexes
Isolated monomorphic premature ventricular complexes (PVCs) without
structural heart disease are generally benign.
► Frequent PVCs can cause reversible cardiomyopathy or aggravate an existing
cardiomyopathy.
► Short coupled PVCs can trigger sustained ventricular fibrillation. These are
often from the Purkinje tissue or rarely the outflow tract.
► Beta blockers are considered first-line therapy but have low efficacy.
Catheter ablation and AADs are reasonable to suppress PVCs in appropriate
patients.
► Ablation is often curative and success depends on location and accessibility
of PVCs.
► Implantable defibrillators are reasonable in patients at higher risk of sudden
cardiac death.
Hemodynamics for the heart failure
This article reviews the role of invasive hemodynamics in the care of patients across the
entire spectrum of human heart failure.
Conceptual principles of ventricular function, ventricular-arterial interaction, load
response, and ventricular interaction in the right and left heart are reviewed.
Principles and practice of invasive exercise testing are provided, along with detailed
discussions on the role of invasive hemodynamics in the evaluation and management of
advanced heart failure, shock, mechanical circulatory support, and pulmonary
hypertension.
Bifurcation stenting
Significant unprotected left main (LM) coronary artery disease is present in <10% of patients undergoing coronary angiography. In autopsy research, a mean LM length of 10.8 mm ± 5.2 mm (range 2–23 mm), mean LM diameter 4.9 mm ± 0.8 mm and mean angle between the left anterior descending (LAD) and left circumflex (LCx) of 86.7° ± 28.8° has been described. This angle value positively correlated with LM length.2 Further studies showed that long LM developed stenoses more frequently near the distal bifurcation compared to near the ostium (77% versus 18%).7 It is also worth emphasising that LM bifurcation disease is rarely focal and that both sides of the carina are almost never disease-free. Furthermore, continuous plaque from the LM into the proximal LAD artery has been reported in 90% of cases.8 Summarised below are the most crucial LM peculiarities (in comparison with non-LM bifurcations), which should be taken into consideration when distal LM stenosis PCI is planned:
Valve in-valve implantation into a failed mechanical prosthetic aortic valve
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Flu Vaccine Alert in Bangalore Karnataka
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Physiology of Special Chemical Sensation of Taste
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Physiology of Chemical Sensation of smell.pdf
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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