Friday, April 3, 2015

DILATED CARDIOMYOPATHY


 
Cardiomyopathy is a term that literally meaning “an ailment of the heart”, used to describe a group of diseases affecting the myocardium, which in response to injury, may undergo dilation or hypertrophy, according to Damjanov (2012),. They are a heterogeneous group of entities affecting the myocardium primarily and not associated with the major causes of cardiac disease, there is now a general agreement on a classification based upon general features of presentation and pathophysiology.  Cardiomyopathy is divided into three forms: Dilated Cardiomyopathy, Hypertrophy Cardiomyopathy, and Restrictive Cardiomyopathy.

Dilated Cardiomyopathy (90% of cases) is considered the most common cardiomyopathy (Le, Bhushan, & Grimm, 2009), also is the third most common cause of heart failure and the most frequent reason for heart transplantation.

It is considered a progressive disease of heart muscle, in which the ventricle are markedly dilated and the heart appears to have a myocardium that is either flabby or thinned and that has been partially replaced  by fibrous tissue, bringing as a  result ventricular chamber enlargement and contractile dysfunction with normal left ventricle wall thickness, the right ventricle may also be dilated (Goswami, 2014). Usually present with symptoms and signs of congestive heart failure, the initial presentation may be severe biventricular failure, accompanied by chest pain and palpitation,  (Tierney, McPhee, & Papadakis, 2005), in the physical examination we find low blood pressure, pulsus alterns, peripheral cyanosis, tachypnea, diffuse apical beat displaced inferolateral and diminished in force, irregularly irregular pulse, as mentioned by Reynolds (2013).

 

Dilated Cardiomyopathy has many causes, but finding a specific cause for an individual case may be difficult, especially as explain Goswami (2014) in patients with multiple risk factors. In many cases (50 % ) of Dilated cardiomyopathy, the cause remains unexplained or idiopathic (Reynolds, 2013). However, some idiopathic causes may result from failure to identify known causes such as infection or toxins, almost a third of cases may result from severe ethanol abuse.

Other causes include:

Genetics, secondary to other cardiovascular diseases, infections, metabolic disorders, nutritional, collagen vascular disease, infiltrative, neuromuscular diseases, primary cardiac tumor, peripartum, and immunologic conditions.

To establish the diagnosis of cardiomyopathy, we must perform a series of complementary studies such as Complete blood count, Metabolic panel, Thyroid function tests, Cardiac biomarkers, B-type natriuretic peptide assay, Chest radiography, Echocardiography, Cardiac magnetic resonance imaging (MRI), and Electrocardiography (ECG) .

As explained by Reynolds (2013) four chamber dilation, decreased global left ventricular systolic and diastolic function, increased left ventricular volumes and left ventricular mass index, with eccentric left ventricular hypertrophy and usually small pericardial effusion are general echocardiographic findings.

Finally the treatment of Dilated cardiomyopathy is essentially the same as treatment of chronic heart failure like a complex clinical syndrome for which many treatment modalities have emerged.

 

Bibliography



Damjanov, I. (2012). Pathology for the Health Professions. Missouri: ELSEVIER Saunders.

Goswami, V. J. (2014, Oct 6). Medscape. Retrieved from emedicine.medscape.com: http://emedicine.medscape.com/article/152696-overview

Le, T., Bhushan, V., & Grimm, L. (2009). FIRST AID for the USMLE step 1. USA: McGraw Hill.

medscape.com. (n.d.). Retrieved from Dilated Cardiomyphaty.

Reynolds, T. (2013). the Echocardiographer's Pocket Reference. Phoenix: Arizona Foundation.

Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2005). CURRENT Medical Diagnosis & Treatment. New York: McGraw Hill.

TRICUSPID REGURGITATION


           
         
Tricuspid Valve as described by Alexander, Schlant, & Fuster (1998) is a complex structure made up of six major anatomic components such as right atrial wall, annulus, three leaflets, chordae tendineae, papillary muscles, and the right ventricular free wall. The three leaflets are named anterior, posterior, and septal.

            Tricuspid Regurgitation (TR) is a disorder in which this valve doesn’t close tight enough resulting in blood to flow backward into the right upper heart chamber when right ventricle contracts, my be acute, chronic or intermittent.

            This disorder may result from structural alterations of any or all of the components of the valve apparatus. According to Mancini (2014), the lesion may be classified as primary when the Tricuspid Regurgitation is caused by an intrinsic abnormality of the valve structure, or secondary when it is caused by right ventricular dilatation. Most of the TR are functional (primary) and secondary of association with severe mitral valve disease, which triggers a marked dilation of the right ventricle, tricuspid ring, and dysfunction of the subvalvular apparatus due to hypertension. As an isolated lesion, is relatively common and caused by infectious endocarditis, preferably between drugs addicts; other possible causes are Ebstein’s disease, atrial septal defect, carcinoid heart disease, and thoracic trauma with papillary muscle rupture (Roca Goderich, 2002).

            Usually well tolerated in the absence of pulmonary hypertension as described Roca Goderich (2002), when the TR is important symptoms like fatigue or asthenia appear, which are related to the decrease of the cardiac output, other symptoms can be edema, hepatomegaly, abdominal distension, jugular venous distension, weight loss, cachexia, cyanosis, jaundice.

            Color Flow Doppler echocardiography is a mainstay for evaluation of TR, other studies are also used: Chest radiography, serum chemistry, ECG, Cardiac catheterization. (Mancini, 2014).

            Doppler techniques are used to directly visualize regurgitation jets, measure the flow velocities of the regurgitate jets, and accurately estimate right ventricular systolic pressure. In trivial to mild TR, the jet is central and narrow, when it progress to severe the width increases as does the penetration of the jet into the right atrium.

            Other possible findings include: Prolapse of the TV, endocarditis, rheumatic heart disease, or Ebstein anomaly, right ventricle dilated, paradoxical motion of the ventricular septum. Using pulsed wave and continuous wave Doppler, right ventricular and pulmonary arterial systolic pressure can be estimated  by measuring the peak regurgitant flow velocity across the tricuspid valve, converting it to a pressure gradient by use of the modified Bernoulli equation, and then adding the gradient to an estimate of the right atrial pressure as mentioned by Ha, Chung, Jang, & Rim, (2000).

            The TR itself does not require intervention; depending on the etiology and severity of tricuspid regurgitation, treatment may involve medication when the TR is secondary to left side heart failure, mild TR associated with mitral valve disease and pulmonary hypertension; or surgical repair or replacement of the valve in cases like Ebstein anomaly, destruction of the valve by bacterial endocarditis, and severe ventricular dilation that is uncontrolled with medical therapy.

 

 


Bibliography



Alexander, R. W., Schlant, R. C., & Fuster, V. (1998). Hurst's The Heart. United States: Mc-Graw Hill.

Ha, J., Chung, N., Jang, Y., & Rim, S. (2000). Tricusp Stenosis and regurgitation: Doppler and color flow achocardiography and cardiac catheterization findings. Clin Cardiol, ;23(1):51-2.

Mancini, M. C. (2014, Jun 2). emedicine.medscape.com. Retrieved from Medscape: http://emedicine.medscape.com/article/158484-overview#a0101

Roca Goderich, R. (2002). Temas de Medicina Interna. La Habana: Ecimed.


Thursday, December 11, 2014

EFFECT OF SUGAR ON INFLAMMATION


Inflammation is a response triggered by damage to living tissues (Encyclopedia Britannica, Inc, 2014), the inflammatory response is a defense mechanism that evolved in higher organisms to protect them from infection and injury.

The injury can be cause by chemical agents, physical forces, living microbes or many other physiologic or pathologic stimuli that disturb the normal steady state as defined by Damjanov (2012), who insists that inflammation occurs only in multicellular organisms that are capable of mountaing a neurovascular and cellular response to injury.

Recent research suggests tha inflammation inside the body plays a role in the development of Type 2 Diabetes. In this condition, the body can’t produce enough insuline or the bodies can’t use the insuline adequately due of insuline resistence (Tierney, McPhee, & Papadakis, 2005).

In a normal condition, when the blood sugar rise rapidly, after some food, the pancreas secretes insulin whose primary purpose is to drive sugar into each cells where it is stored for energy. If the cells is full, it is rejected, them blood sugar rise again producing more insuline and the glucose converts to stored fat, as Dr Lundell (2012) explain, the extra sugar molecules attach to a variety of proteins that in turn injure the blood vassels wall and set off the inflammation.

In the other hand, inflammation is induced by chemical mediator produced by damage host cells, such as Cytokines (Beck, 2014) and others, the bolus of blood sugar that accompanies a meals or snack of highly refined carbohydrates like bread, white rice, French fries, sugar laden soda, increases levels of this inflammatory messenger (President & Fellows of Harvard College, 2007). Researchers discovered that in people with type 2 diabetes, cytokine levels are elevated inside fat tissue, causing low levels of abnormal inflammation that alter the action of insulin and contribute to development of the disease (Nazario, 2012) the body becomes less sensitive to insulin and the resulting insulin resistance also leads to inflammation. A vicious cycle can result, with more inflammation causing more insulin resistance and vice versa.

Spranger, et al.(2002) evaluated the effects of various inflamatory cytokines on the risk of type 2 diabetes and they concluded supporting the concept that subclinical activation of the immune system is involved in the pathogenesis of type 2 diabetes, demonstrating in their study that a specific pattern of cytokines was associated with an increased risk of type 2 diabetes, rather than isolated elevation of the respective cytokines.

Finally, although there is no clearly in the pathogenic mechanism, several studies demonstrating the association between elevated blood sugar levels, inflammation and diabetes mellitus, we are only in the beginning to understand the role of this form of internal inflammation may play in the development of chronic diseases like diabetes and vice versa.
Bibliography
Beck, S. (2014, 11 10). hopkinsmedicine.org. Retrieved from Acute and Chronic inflamation: https://www.google.com/?gws_rd=ssl#q=sarah+beck+acute+inflammation
Danjanov, I. (2012). Pathologic fro the Health Professions. ELSEVIER.
Encyclopedia Britannica, Inc. (2014, April 11). www.britannica.com. Retrieved from Encyclopaedia Britannica: http://www.britannica.com/EBchecked/topic/287677/inflammation
Lundell, D. (2012, Mar 1). www.sott.net. Retrieved from Heart Surgeon speaks out on what really causes heart disease: http://www.sott.net/article/242516
Nazario, B. (2012, Aug 10). www.wedMD.com. Retrieved from http://www.wedmd.com/diabetes/guides/inflammation
President & Fellows of Harvard College. (2007, february). www.health.harvard.edu. Retrieved from The Harvard Medical School: http://www.health.harvard.edu/fhg/updates/What-you-eat-can-fuel-or-cool-inflammation-a-key-driver-of-heart-disease-diabetes-and-other-chronic-conditions.shtml
Spranger, J., Kroke, A., Mohlig, M., Hoffmann, K., Bergmann, M., Ristow, M., . . . Pfeiffer, A. (2002, Jul 26). www.diabetes.diabetesjournals.org. Retrieved from American Diabetes Association: http://diabetes.diabetesjournals.org/content/52/3/812.long
Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2005). CURRENT Medical Diagnosis & Treatment. McGraw Hill.
 


 

HEART SURGEON SPEAKS OUT ON WHAT REALLY CAUSES HEART DISEASE


Dr Dwight Lundell said, “I freely admit to being wrong…..today is my day to right the wrong with medical and scientific fact….insisted heart diseased resulted from the simple fact of elevated blood cholesterol….the only accepted therapy was prescribing medications to lower cholesterol and diet that severely restricted fat intake….It is not working”.

I think this is a statement with a dramatic picturesque approach, before at all, cardiovascular disease can refer to differents heart or blood vessel problems, the term is often used to mean damage to your heart or blood vessels by atherosclerosis, a buildup of fatty plaques in your arteries, it buildup thickens and stiffens artery walls, which can inhibit blood flow through your arteries to your organs and tissues (Mayo Clinic Foundation, 2014).

Atherosclerosis is the most common cause of cardiovascular disease, but it can be caused by others correctable problems such as unhealthy diet, sedentary, obesity and smoking. Hyperlipidemia, included the high blood cholesterol, constitutes one of the most important risk factors for atherosclerosis (Damjanov, 2012) and cardiovascular diseases.

The discovery a few years ago that inflammation as concept, in the artery wall is the real cause of heart disease like Dr Lundell mentions,  is really true, but a long time ago, the medical community in spite of an incompletely understood the interaction between the critical cellular elements in the atherosclerotic lesion, postulated theories related to atherosclerosis and cells injury, for example Rokitansky in 1851, suggested that atherosclerosis begins in the intima with deposition of thrombus and its subsequent organization by the infiltration of fibroblasts and secondary lipid deposition, few years later in 1856, Virchow proposed that atherosclerosis start with lipid transudation into the arterial wall and its interaction with cellular and extracellular elements, causing intimal proliferation (Boudi, 2014). In the 1990s, Ross and Fuster postulated that vascular injury starts the atherosclerotic process. (Ross, Fuster, & Topol, 1996).

The above explained that we were not wrong, but we were finding explanations based on studies and investigations that were conducted.

Finally, with the knowledge that we have today, the concept a little clearer about the inflammation and potential precursors, I agree with Dr Lundell, what we can do is choose whole foods that our grandmother served and not the manufactured foods that we found in the grocery today, because eliminating inflammatory foods and adding essential nutrients from fresh unprocessed food, we can reverse the damage in our arteries.

Bibliography

Boudi, F. B. (2014, May 12). www.emedicine.medscape.com. Retrieved from Coronary Artery Atherosclerosis: http://emedicine.medscape.com/article/153647-overview#aw2aab6b2b

Damjanov, I. (2012). Pathology for the Health Professions. ELSEVIER.

Mayo Clinic Foundation. (2014, Jul 29). www.mayoclinic.org. Retrieved from Heart Disease: http://www.mayoclinic.org/diseases-conditions/heart-disease/basics/causes/con-20034056

Ross, R., Fuster, V., & Topol, E. (1996). Atherosclerosis and Coronary Artery Disease. Philadelphia, PA: Lippincott-Raven.