Anti-oxidant and Anti-tumor properties in Purslane

Purslane is a weed extensively used as edible plant and also acts as antioxidant and anti-tumor agent. A study revealed that PSO (Purslane seed oil) is having remarkable free radical scavenging capabilities and also displayed anti-proliferative effect on MCF-7 cells than on Hela or Eca-109 cells, based on time and dose-dependent manner. PSO is a healthy food for the prevention and controlling hypersensitive symptoms. Further research is needed to understand the anti-tumor and anti- oxidant mechanisms.Purslane (Portulaca oleracea L.) is a widely distributed weed that is extensively used not only as an edible plant but also as a traditional Chinese herbal medicine. Both the leaves and seeds of purslane can be consumed orally or applied topically to soothe a skin allergy. Many studies have demonstrated various pharmacological effects of this plant, such as antibacterial hypoglycemic,anti-hypoxia antioxidant effects, antitumor activity,  and neuroprotective effects. 

As a medicinal and edible wild plant, purslane is generally known as a “longevity food” due toits reputation as a “natural antibiotic”. Purslane contains many compounds, including flavonoids,alkaloids, omega-3 fatty acids, noradrenaline, alkaloids, coumarins, flavonoids, polysaccharides, and other active ingredients. In particular, purslane seeds are reportedly more effective in antioxidation than those from other herbs. In previous studies, we have extracted purslane seed oil (PSO) with a 17.68% yield using an ultrasound-assisted enzyme hydrolysis combined with a Soxhlet extraction method. We then analyzed the fatty acid profile and content of the oil using a Gas Chromatography-Mass Spectrometer (GC-MS). Analysis of the PSO showed that alpha-linolenic acid reached 40.2570% followed by linoleic acid (29.4308%) and oleic acid (15.6103%). Saturated fatty acids represent 13.9455% of the total oil, while monounsaturated fatty acids and polyunsaturated fatty acids (PUFAs) account for 16.2877% and 69.6878%, respectively. Read more...............

De Bukes Syndrome - Tetrology of Fallot with Absent Left Pulmonary Artery

De Buckes syndrome – TOF with unilateral absence of a pulmonary artery (UAPA) is a rare condition with an estimated prevalence of 1 in 200,000 young adults . Most commonly, UAPA occurs in conjunction with cardiovascular abnormalities such as tetralogy of Fallot (TOF) coarctation of the aorta, VSD, subvalvular aortic stenosis, transposition of the great arteries (plus VSD or pulmonary stenosis), Taussig-Bing malformation and coarctation, congenitally corrected transposition and pulmonary stenosis, scimitar syndrome. Patients with isolated UAPA can remain asymptomatic into late adulthood but usually report symptoms such as dyspnea or chest pain or suffer from hemoptysis or recurrent infections. Diagnosis can be difficult due to the rarity of the condition and its nonspecific presentation. We present a case of a 5month old child who presented with TOF with Right pulmonary artery stenosis and absent left pulmonary artery, with typical findings on chest radiograph, angiographic features and treatment discussed.

Case Report: A five months old male child was referred to Sri Jayadeva Institute of Cardiovascular Science and research for cardiac evaluation. He was born to non-consanginous parents with normal pregnancy and normal delivery. He presented with history of incessant feeding and cyanosis while feeding and crying. On physical examination, the patient had cyanosis with SpO2 of 67%. There was no respiratory distress at rest. His weight was 3 kgs (just below the 5th percentile for his age). Heart rate was 104 beats/minute and blood pressure was 100/55 mmHg. Cardiovascular examination revealed normal peripheral pulses, the second heart sound was single and Grade 3/6 Ejection systolic murmer. The electrocardiogram showed sinus rhythm, right axis deviation and right ventricular (RV) hypertrophy. Chest X-ray showed mild cardiomegaly, with normal bronchovascular markings on right side and absent bronchovascular markings on left side. Read more.......... 

Serum-Soluble CD40 Ligand Level in MPO-ANCA-Associated Renal Vasculitis

In antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), the diagnostic value of assays for ANCAs is now widely accepted. ANCAs are known to bind two key antigens found in neutrophil granules and monocyte lysosomes: proteinase-3 (PR3) and myeloperoxidase (MPO). ANCAs can activatecytokine-primed neutrophils, causing an oxidative burst, degranulation, therelease of inflammatory cytokines, and damage to endothelial cells in vitro,and an intravenous injection of mouse antibodies specific for mouse MPO induced pauci-immune necrotizing and crescentic glomerulonephritis in a mouse model that closely mimics the human disease. The pathogenicity of anti-MPO antibodies has been demonstrated in vitro and in vivo , but the mechanisms of MPO-ANCA production have not been clarified. Moreover, the MPO-ANCA titer is not always associated with disease activity.

The interaction between CD40 and its ligand (CD40L) is critical to the control of thymus-dependent humoral immunity and cell-mediated immune responses. CD40L on the T cells stimulates the B-cell secretion of immunoglobulin isotypes in the presence of cytokines. The interaction of CD40L with CD40 not only induces a proliferation of B lymphocytes and their isotype switching; it also mediates a broad variety of other immune and inflammatory responses. CD40 signaling has been linked with pathogenic processes of chronic inflammatory diseases such as autoimmune diseases, neurodegenerative disorders and graft-versus-host disease. Soluble forms of CD40L, produced by proteolytic cleavage, lack the transmembrane region and a portion of the extracellular domain, but they contain the entire tumor necrosis. Read more............

Failure of Ventricular Capture and Pacemaker Exit Block Secondary to Moderate Hyperkalemia

Hyperkalemia is a life threatening metabolic condition. When the K level increases, the intraventricular conduction velocity is decreased and the paced QRS complex widens. When the K level reaches 7 mEq/L pacing thresholds could increase, with or without increased latency. Occasionally failure to capture appears at a lower level, especially in the presence of heart disease. We report a case where moderate hyperkalemia caused pacemaker exit block and a failure of ventricular pacemaker capture. An 81-year-old woman was admitted to our institution with bradycardia, weaknessand presyncope. She had a history of type 2 diabetes mellitus and chronic kidney disease (eGFR of 12 ml/min). Patient underwent bivalvular mechanic mitral- aortic valve replacement 13 years ago. 

Six months after cardiac surgery the patient underwent a VVI pacemaker implant (Vitatron G20) for permanent atrial fibrillation with slow ventricular response. The patient’s pacemaker was programmed VVI with a lower rate limit 70 beats/min. In the last weeks, congestive heart failure symptoms had appeared, thus loop diuretic dose was increased (Furosemide 100 mg per day). Her medications also included digoxin 0.25 mg per day, warfarin 2 mg per day, and insulin; thus she didn’t take antiarrhythmic drugs at admission physical examination revealed a pulse rate of 42 per minute, blood pressure of 95/50 mmHg, and an oxygen saturation of 93% on room air with a respiratory rate of 24. Signs and symptoms of acute heart failure were present.Read more............

Titan™ sensor a potential hemodynamic monitor or not

Heart failure is a common problem and long term monitoring of heart function accurately in patients has gained increased interest. A study was carried out in 40 patients to test the safety and feasibility of Titan™ pressure sensor. Titan™ sensor is small, resembling the CardioMEMS® device . Titan™ is implanted principally in any heart chambers, recently for the first time modified device of Titan™ was implemented viacatheter in animals and good results were observed. The first study in man on a new implanted wireless hemodynamic monitor showed favourable results.

Heart failure is a huge health problem. The disease often follows a similar course; stable in the initial stages but progressive deterioration develops with exacerbations that eventually lead to recurrent hospitalization. To begin with, patients usually respond to standard medical treatment, but the course is unpredictable and in the final stages inotropic support is often required to preserve life.The possibility of monitoring heart function more accurately in these patients has gained increasing interest. The ability to detect a sudden increase in filling pressure would provide early warning of an imminent exacerbation and enable medical intervention before the development of clinical symptoms .

There are a few implantable cardiac hemodynamic monitors on the market, some already in use while others have gone through clinical studies with successful safety records. These devices can be divided into two categories; those monitoring pressure of the left side of the heart, and those on the right.A catheter-based technology with a device introduced into the pulmonary artery allowing wireless recordings of pulmonary artery pressure and indirectly pulmonary artery wedge pressure is currently approved by the Food and Drug Administration. Read more.............

Perivascular Adipose Tissue can be Considered a Risk Factor for Atherosclerosis?

Perivascular adipose tissue (PVAT) is an ectopic deposition of adipose tissue surrounding the vasculature and your influence on the vasculature changes with increasing adiposity. PVAT involves coronary arteries, aorta, mesenteric, and small arteries in the body, and its likely function differs in each of these anatomical regions .

PVATsecretes a wide variety of adipocytokines and other substances, includinghormones, cytokines, chemokines, oxygen radicals, angiotensinogen, leptin,resistin and fatty acids. The rate of secretion of various adipocytokines varies in different places in the vascular tree, adipocytokines as TNF-α, IL-6 and others. Adiponectin can affect insulin sensitivity, inflammatory responses, hemostasis, appetite and atherosclerosis. The factors secreted by PVAT that act in the regulation of vascular function.

PVAT is related to the vascular contractility, endothelial dysfunction, neointima formation, arterial stiffness, aneurysm formation, and produce substances that can interfere in the process of atherosclerosis and contribute to the pathogenesis of type 2 diabetes and cardiovascular diseases .

An understanding of the pathophysiology of PVAT and its potential role in cardiovascular morbidity and mortality can be significant in preventing and treating of atherosclerosis. Read more.......

Cardiovascular Risk in Rheumatoid Arthritis. An Update for General Practitioners

A review must rely on solid data, be objective and deliver the ‘state of the art’ of the argument. The quest is a seemingly endless process. Writing is a solitary endeavor but data depend on the work of many individuals and institutions. We started a goal-oriented search in English and German with the engines BioMedSearch.com, Cardio source, Center Watch, ClinicalTrials.gov, Cochrane, Google Scholar, Med Watch, Research Gate and PubMed. We settled atime-window 2000-2016 with key words: RA, arthritis, cardiovascular risk in RA,and treatment of RA. Our search delivered more than 1 million of references. 

The filter was restricted to guidelines and meta-analyses. This search delivered more than 80,000 references. Using a plagiarism’s software we found that few centers published more than 60% of the collected references, usually changing authors’ order, deleting or adding some authors. Many papers present strikingly similar data. Many authors quote their previous publications. One might maliciously say that these authors repeated data in different journals using their references in order to increase their scientific impact factor. We selected papers with large numbers of cases and ended with a total of 340 references. From the abstracts we selected 166 full-text papers. Ninety-three papers sufficed to get the ‘state of the art’ of cardiovascular complications (CV) in RA. It is unavoidable that we may have either selected or omitted same papers by chance. Read more.............

Is it possible to prevent prevention of Preeclampsia?

Preeclampsia (PE) is one of the pregnancy related disorders; it is not clearly evident due to its complex signs and symptoms. It causes morbidity and mortality in women. Even the advanced research practised to reduce the morbidity and mortality has failed because of the multifactorial origin of the pathogenic process. Even developing a single biomarker for PE is difficult because of its heterogenecity. Initially anti-hypertensive drugs were used as it is the main symptom of PE but these drugs did not give any positive results. Some of the other drugs for PE includes calcium supplement,Acetylsalicylic acid etcbut are not up to the mark.

Preeclampsia (PE) involves dysfunction in pregnancy, with consequences of morbidity andmortality worldwide. The prevalence of PE is 5% to 8%. PE is characterized by systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg as assessed on two occasions at least 4 hours apart. Additionally, PE is also characterized as the presence of proteinuria of >300 mg per 24 hours or when urinary dipstick proteinuria is ≥ 1, after 20 weeks of pregnancy, or in the absence of proteinuria, the first appearance of thrombocytopenia. PE is one of the major causes of maternal mortality, resulting in 50,000 to 60,000 deaths annually worldwide. This disease also increases the risk of complications in the mother and development of cardiovascular disease in later life in the newborn and the mother.Read more.............

Dysostosis Multiplex (Gm-1 Gangliosidosis: Type II)

GM1 gangliosidosis is an autosomal recessive lysosomal storage disorder characterized by the generalized accumulation of GM1 ganglioside, oligosaccharides, and the mucopolysaccharidekeratan sulfate (and their derivatives). Deficiency of the lysosomal hydrolase, acid β-galactosidase, causes GM1 gangliosidosis . GM1 gangliosidosis is a rare disorder, and theestimated incidence is 1:100,000-200,000 live births. GM1 gangliosidosis is found in all races, although specific alleles can be identified in certain ethnic groups. A high frequency of GM1 gangliosidosis has been reported from Southern Brazil, and a large number of Japanese patients with the adult form have been reported. All 3 types of GM1 gangliosidosis are inherited as autosomal recessive traits and have equal sex distributions.

5 years old boy with normal birth history born to a nonconsanginous parents, presented with mild developmental delay, gait difficulties and stiffness of limbs since 4 year of age. Initially parents noticed child had tiptoe walking, later he had stiffness of both upper and lower limbs which is gradually progressive. Child is still able to walk but unable to run. There is history of febrile seizures at 1.5 year of age. Younger sibling also having similar complaints

On examination:Boy is alert, cooperative GPE revealed, Coarse facial features, proptosis, prominent forehead, tented upper lip, hepatosplenomegaly, melanotic patches over back, elbow, finger & hamstrings contracture, protrubrent abdomen with umbilical hernia, brisk reflexes, power 5/5 and spastic gait.Investigations: CBC showed normocytic hypochromic with mild relative monocytosis, LFT’ & RFT’s were normal, Urine test positive for MPS, Serum Hexosaminidase. A enzyme levels raised above normal limits, Aryl sulfatase negative, Beta galactosidase enzyme levels were reduced. Read more........

Recurrence of Permanent Junctional Re-entry Tachycardia: Indication for Ablation of the Junctional Pathway

Echocardiography showed a severe dilatation of the left ventricle of 6.8 cm and a severe reduction of left ventricular function with an ejection fraction of 28%. Furthermore, moderate mitral and tricuspid regurgitation was documented.After two days resuming of the prior dosage of bisoprolol, the patient still was in incessant permanent junctional re-entry tachycardia, which lead to dramatic deterioration of left ventricular function. This patient was send home and was booked for radiofrequency ablation in an electrophysiological laboratory not far away.

PJRT is a potentially lethal arrhythmia in children and in adolescants with tachycardia induced cardiomyopathy. Although rarely reported, spontaneous resolution is not uncommon. Antiarrhythmic treatment is often effective,especially with amiodarone and verapamil. Radiofrequency ablation should be reserved for older patients and especially in patients with persistent left ventricular dysfunction.Radiofrequency ablation of this particular accessory pathway remains an intervention at high risk of requiring permanent pacemaker implantation because of its proximity to the septum. The primary ablation success rate is 92%, but the recurrence rate after 9 months is 29% for cryoablation and 8.6% for radiofrequency ablation. Read more.............

The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodeling.

Myocardial infarction (MI), commonly known as heart attack, is a major public health problem. MI can result in a maladaptive remodeling of left ventricles (LV) that leads to LV dysfunction and eventual heart failure. The acute mortality of MI is decreasing due to improved managements and treatment strategies including early coronary reperfusion therapy. However, the prevalence of heart failure as a result of a maladaptive post-MI LV remodeling is still steadily increasing. The cardiovascular risk for patients with MI is still 10-fold higher thanhealthy human. Consequently, the morbidity, mortality, and economic cost related to ischemic heart disease are rising worldwide.

Because the heart has limited regenerative capacity, it responds to MI injury by a spontaneous wound repair process which ultimately results in replacement of dead cardiomyocytes with a collagen-based scar. Wound healing is closely intertwined with ventricular remodeling, a complex process that involves both the infarcted and non-infarcted myocardium, and leads to alteration in the size, shape, and physiology of the heart. The extent of post-MI remodeling is an important predictor for mortality of heart failure after infarction, and depends on the size of the infarct and on the mechanical and structural characteristics of the healing wound. Read more......

A Rare Case of Retrograde Aortic Balloon Valvuloplasty in a Neonate with LV Dysfunction

A 25 day old male neonate presented to our institution with excessive sweating during feeds since few days after birth. On examination the neonate appeared weak with decreased feeding (Weight 2.8 kg). He was tachypneic with feeble pulses. There was no hepatomegaly. Cardiovascular examination revealed cardiomegaly, vulvar ejection click and an ejection systolic murmur of aortic stenosis. Left ventricular hypertrophy was recorded in the ECG and the chest X-ray showed cardiac enlargement. Two dimensional echocardiography revealed an enlarged hypertrophied left ventricle with reduced left ventricular function and a tricuspid aortic valve with systolic doming. A gradient of 102 mm Hg was recorded on Doppler examination.

After obtaining informed written consent for BAV the recorded baseline hemodynamic data suggested severe valvular AS with an aortic valve gradient of 108 mg Hg. We dilated the aortic valve using a 10 mm balloon (annulus size 10 mm) mounted on a 5 French catheter passed percutaneous via the right femoral artery. Theresult gradient across the aortic valve was 54 mm Hg. The procedure was uneventful except for transient ectopic during balloon dilatations. At the time of discharge the infant was feeding well without head sweats. Short term fallow up revealed favourable outcome.The optimal management for critical aortic stenosis in early infancy continues to challenge cardiologists and cardiac surgeons. Trans catheter aortic balloon valvuloplasty has become the first-line treatment for critical aortic stenosis (AS) in neonates. However, need to know more about the growth and function of left heart structures or about patterns of re-intervention on the left heart after neonatal aortic balloon valvuloplasty.  Read more.....

Toward Precision Therapy in ANCA-Associated Vasculitides

The diagnosis of anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) is often made in a context of emergency, and relies on clinical presentation, positivity of ANCA antibodies and/or histological documentation. The severity of residual organ damage, in particular chronic kidney disease (CKD), depends on the precocity of diagnosis, the efficacy of induction treatment, and on the prevention of AAV relapses. Recently, although targeted therapy with rituximab have shown efficacy for the induction and maintenance  of remission in AAV, residual organ damage and infectious complications are still penalizing patients. The identification of reliable biomarkers could help personalize the level and/or duration of immunosuppression (i.e., precision medicine).

Indeed, type and severity of organ involvement are heterogenous among patients, and ANCA positivity can be missing in patients with granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA) andeosinophilic granulomatosis with polyangiitis (EGPA). During follow-up, an increase in proteinuria or an impairment of renal function can result from chronic kidney disease progression, or from necrotizing pauci-immune crescentic glomerulonephritis, so that chronic renal lesions can be difficult to clinically discriminate from active vasculitis flare. In such setting, renal biopsy is a valuable tool but remains an invasive procedure that cannot be repeated easily. 

The follow-up of ANCA positivity and of anti-proteinase 3 (PR3) or anti-myeloperoxidase (MPO) antibodies titers is, to date, the most accurate biomarker available to evaluate disease activity and/or predict relapses. Although several studies converge to show that severe flares were very unlikely in patients with negative ANCA, the clinical utility of ANCA follow-up to predict relapses is still debated, and no preemptive increase in immunosupresssion is currently recommended in patients showing new ANCA positivity or a rise in anti-PR3/anti-MPO titer. 

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Novel Cell Replacement Strategies for Heart Failure Treatment

Myocardial infarction (MI), or heart attack, is caused by the blockage of blood flow in the heart, which reduces oxygen levels, damages tissues (ischemia) and kills close to one billion cardiomyocytes (infarction). Fibroblasts then migrate into the infarctedarea where they proliferate to create a cardiomyocytedepleted scar that cannotcontribute to the electrophysiologicallydriven contractions of the heart. This often causes HF leading to fatigue, peripheral edema, or even death. To find more effective therapies for HF, we need to improve our understanding of its pathophysiology and develop new approaches to treating it.

Cell-replacement therapy has emerged as a novel approach to treat HF. This approach relies on the theory that after MI or in HF, lost cardiomyocytes can be replaced by adding either new cardiomyocytes or a potential source of cardiomyocytes such as stem cells. To find the most effective approach, researchers have tested several types of stem cells including skeletal myoblasts, cardiac progenitor cells, and mesenchymal stem cells from bone marrow. However, they have only been modestly successful because the beneficial effects are mainly mediated by indirect paracrine mechanisms: stem cells do not transdifferentiate into cardiomyocytes in-vivo and the number of stem cells retained in the heart after delivery is disappointingly low. 

Fortunately, cell-replacement therapy for HF using pluripotent stemcell- derived cardiomyocytes showed more promising results in rodents and non-human primates because they integrate and electrically couple with the healthy myocardium. However, technologies involving stem-cell-derived cardiomyocytes must be further optimized before they can effectively treat HF. Specifically, we need to find methods that improve the efficiency and consistency of cardiomyocyte differentiation in large scale, their survival in disease conditions, their integration into cardiac tissue, and their resistance to autoimmune rejection.

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Cardiovascular Risk in Rheumatoid Arthritis. An Update for General Practitioners

Rheumatoid arthritis (RA) is a chronic inflammatory joint pathology which affects almost 1% of the general population and which is ranked among the top 15% of diseasescausing major disability worldwide. RA shares several pathophysiologicfeatures, genetic predisposition and risk factors with atherosclerosis. Inflammation is the central pathologic factor in both diseases. The paper reviews cardiovascular events and their therapy in RA.

Methodology:

A review must rely on solid data, be objective and deliver the ‘state of the art’ of the argument. The quest is a seemingly endless process. Writing is a solitary endeavor but data depend on the work of many individuals and institutions. We started a goal-oriented search in English and German with the engines BioMedSearch.com, Cardio source, Center Watch, ClinicalTrials.gov, Cochrane, Google Scholar, Med Watch, Research Gate and PubMed. We settled a time-window 2000-2016 with key words: RA, arthritis, cardiovascular risk in RA, and treatment of RA. Our search delivered more than 1 million of references. The filter was restricted to guidelines and meta-analyses. This search delivered more than 80,000 references. Using a plagiarism’s software we found that few centers published more than 60% of the collected references, usually changing authors’ order, deleting or adding some authors. Many papers present strikingly similar data. 

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Radiation-Induced Arterial Injury in the Upper Limb

RIAI was first reported by Thomas as a condition in which radiation therapy causes stenosis and obstruction of the great vessels. Incidence and prevalence of radiation induced subclavian artery stenosisTo date, it has been considered that RIAI is rare after radiation therapy. However, because of advanced imaging technology and the fact that clinicians have become aware of the concept of RIAI, reports of RIAI have increased.

Lam compared newly diagnosed patients with nasopharyngeal cancer patients before and after they underwent radiation therapy and reported that arterial stenosis was more common in the irradiated area of the post-radiation group compared with that of the pre-radiation group(56/71 vs. 11/51). Furthermore, arterial stenosis of 50% or more was only observed following radiation therapy.In addition, the probability of carotid stenosis of 70% or more after radiation therapy is 6.3% according to Elerding and 11.7%–16% according to Cheng. It is also reported that the symptom due to this vascular stenosis appears in 14.6% of the cases. 

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Complications of Pharmacological Spasm Provocation Tests

As pharmacological spasm provocation tests, acetylcholine (ACh) and ergonovine (ER) are employed in the cardiac catheterization laboratory. However, we often encounter the major and minor complications during performing these procedures. As a diagnostic tool, we should perform spasm provocation tests more safely without major complications. Multiple and proximal spasm documented by the pharmacological agents may occur a hemodynamic instability, such as shock and hypotension. Moreover, irreversible arrhythmia may be recognized. Selective spasmprovocation tests such as intracoronary injection of ACh and ER is safer than the intravenous injection of ER. The effect time of ACh is very short and we may have the spontaneous remission of the provoked spasm. Therefore, we can perform a selective right and left coronary artery testing separately. We already reported the major complications during ACh spasm provocation tests in 2000.

Serious major complications were not different from the reports with an intravenous injection of ER. Recently, we employed the sequential spasm provocation tests to document coronary spasm in the clinic . As sequential spasm provocation tests, we first perform intracoronary injection of ACh, second intracoronary administration of ER, and finally adding intracoronary injection of ACh just after ER test if we did not obtain the provoked spasm. However, the majority of cardiologists employed a single spasm provocation test for example ACh alone or ER only in each institution. 

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Cardiac Ischemia and Angina Pectoris without Flow-Limiting Coronary Artery Disease (Coronary Syndrome X)

Coronary ischemic disease (CID) is a worldwide frequent pathology with increasing prevalence. Angina pectoris (AP) is a cardinal symptom of CID. Typical AP meets all of the following criteria: retrosternal chest discomfort of characteristic quality and duration; provoked by exertional or emotional stress; is relieved by rest and/or nitrates within minutes.

It was stated that ‘no patient with AP failed to show occlusion in at least one of the major coronary arteries’ and flow-limiting coronary artery disease (CAD) causing ischemia was accepted as the cause of AP. However, this assumption is not unconditional because AP may also occur in other diseases, such as e.g. hypertrophic cardiomyopathy, severe aortic stenosis, profound anemia, and carboxy hemoglobin intoxication.

In 1967 two papers described patients with typical AP and sometimes dyspnea and neurovegetative symptoms (e.g. perspiration, tachycardia and dizziness) without epicardial CAD (CAD). This cardiac pathology is usually called cardiac 

syndrome X (CSX) and is not rare.

Case Report

A 53-year old Caucasian woman had stable typical AP which was questionably relieved by sublingual nitroglycerin. Her father died at the age of 55 years because of acute myocardial infarction. The patient had no other cardiovascular risk factors. The resting ECG showed ischemic changes. Plasma levels of troponin, measured during and several hours after episodes of AP, were not increased. Echocardiography detected only a moderately impaired left ventricular relaxation.  Read more..............

A New Way for Spreading Knowledge in Vasculitis

In clinical practice, vasculitides are often regarded as extremely rare diseases, that unfortunately sometimes residents and fellows are discouraged to give much attention to these disorders, instead they ought to prioritize more common diseases in their studies. Vasculitis is a group of heterogeneous and protean disorders that pose as a major challenge for internists and physicians from different medical specialties. Diagnosing a vasculitis may also be an important challenge for rheumatologists who are not familiar with this fascinating group of multi organ/system diseases.

Indeed, multiple conditions do mimic manifestations of vasculitis and are usually more prevalent than vasculitis per Although, the onset of most systemic vasculitides is subacute, the lack of suspicion of a vasculitis in a severely ill patient who actually present a systemic vasculitis is potentially harmful and may result in significant morbidity or even in an increased risk of death. It is important to emphasize that attempts should always be made to confirm diagnosis of suspicious cases of vasculitis with appropriate methods that include imaging studies (e.g. angiography for large and medium vessel vasculitis), pathology assessment of affected tissue for small-vessel vasculitis or serologic tests (e.g. antineutrophil cytoplasmic antibodies, anti-C1q antibodies or cryoglobulins).

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Mitral Valve Repair in a Patient with Hereditary Haemorrhagic Telangiectasia

Hereditary hemorrhagic telangiectasia (HHT), also known as Osler–Weber–Rendu syndrome and Osler disease , is an autosomal dominant genetic disorder that leads to abnormal blood vesselformation in the skin, mucous membranes, and affects vital organs such as thelungs, liver, and brain. The disease carries the names of Sir William Osler, Henri Jules Louis Marie Rendu, and Frederick Parkes Weber, who described this condition in the late 19th and early 20th centuries.

This may lead to epistaxis, hemoptysis, intracranial bleeding and gastrointestinal tract bleeding. Treatment focuses on controlling bleeding and other targeted interventions such as surgery, laser therapy and endovascular interventions to remove arteriovenous malformations in organs. In cardiac surgery, the number of reported cases with Osler’s disease remains small. We reported this complicated case of HHT with mitral valve regurgitation that was successfully treated by mitral valve repair.

Case Report:

A 65 year old man was diagnosed with severe mitral regurgitation when he attended his General Practitioner with exercise related dyspnoea. Echocardiography confirmed the presence of leaflet prolapse. When aged 63, he was diagnosed with HHT after experiencing several episodes of epistaxis. Other current medical history included polymyositis rheumatica and asthma. His medication included tranexamic acid 100 mg three times a day, prednisolone 15 mg once daily, thalidomide 50mg once daily, salbutamol inhaler four times a day and Calcium and Iron supplement. Read more......

Complete Heart Block as a Presentation of Viral Myocarditis

Background: An acquired complete heart block is not common in previously healthy children. Underlying causes and the treatment of the acquired heart block would provide the different outcome.

Methods: Retrospective review of two recent cases of acquired complete heart block in children reported in relation to viral myocarditis.

Result: Two pediatric cases were referred to our facility due to the complete heart block after they initially presented with low cardiac output symptoms. Both of those children were implanted with temporary pacemaker and were administered with intravenous immunoglobulin. Their complete heart blocks recovered within 72 hours of treatment while their ventricular functions were gradually improved.

Conclusion: Acquired complete heart block related to the viral myocarditis in children is reversible despite the initial clinical presentation which is potentially rapid in its onset and progressive with potentially fatal outcome.  Read more