A case of arrhythmia

50-year old male patient came to our hospital complaining of palpitations. He had steted that the onset was about 45 minutes ago and was relater to a fall from a ladder. The patient showed no dyspnea or chest pain. He was not on any medications. There was no signs of distress. His BP was 100/60 and heart rate was 140 bpm and irrregularly irregular. 12-lead ECG was done and here it is:
Click on it to enlarge







What do you thin is the diagnosis and what should we do?


Update: see the tracing after cardioversion below

Uncommon case of chest pain CME on medscape

Here is a new CME case from CME medscape.
It is a nice case of chest pain due to an uncommon cause. Just try to guess the answer without looking at the multiple choices at the bottom and see if you can expect it. Look carefully in the X-ray. The link is here.

http://cme.medscape.com/viewarticle/702661

Statins

• Members:

- Atorvastatin
- Lovastatin
- Fluvastatin
- Pravastatin
- Simvastatin
- Rosuvastatin

• Chemistry:

Simvasatin and Lovastatin are prodrugs containing lactone ring which is hydrolysed in the GIT into beta-hydroxy derivatives. Pravastatin is active as given as it has an open lactone ring.
Atorvastatin, Fluvastatin and Rosuvastatin are fluorine containing cogeners and are also active as given.

• Pharmacokinetics:

Absorption: variable from 40 - 75 %. Only Fluvastatin is absorbed 100%. All members are susciptible to 1st pass metabolism.

Excretion: Mainly hepatic excretion in bile. Only 5 -20 % are excreted in urine.

Half-life: Atorvastatin and Rosuvastatin have relatively long half-lives (14 and 19 hours respectively). Others agents have short half-lives (1-3 hours).

• Mechanism of action:

Competetive inhibition of the enzyme HMG-CoA reductase, which is the key enzyme in cholesterol synthesis (it catalyzes the rate limiting reaction). This causes marked reduction in LDL-cholesterol level, elevation of HDL-cholesterol level and slight reduction in triglycerides level.

There is also some other actions (most are of unknown mechanisms) that do not depend on the lipid lowering effect of statins. These are called "pleotropic" actions and they include:

1. inhibition of the inflammatory response.
2. improvement in the endothelial function.
3. platelet stabilization.
4. fibrinogen lowering effect

• Adverse effects:

1. GIT disturbances: in the form of nausea, abdominal colic, diarrhea or constipation and flatulence.
2. Headache.
3. Pruritus.
4. Fatigue, myalgia or even myopathy can occur with statins. It is advisable to do CK level and stop statin if the level is 10-times the normal. The addition of oral coenzyme Q10 may decrease the symptoms. If the patient has developped myopathy, stop the statins and rechallenge later on with lower dose. It may be preferable to shift to Simvastatin or Fluvastatin which has lower incidence of myopathy. If the symptoms recurred, statins should be avoided and non-statin lipid modifying drugs are used instead.
5. Liver damage: it is a serious but rare side effect. transaminase level should be measured before starting treatment and after 3 months of initiation of statins. Later on, semiannual liver enzymes are advised. Elevation of liver enzymes to 3-folds the baseline is an indication to stop statins.
6. Drug interactions: Pravastatin and Fluvastatins are not metabolized by ctochrome oxidase P450, so, they are not susciptible to major drug interactions. Other agents are dependent on this enzyme for their metabolism. Enzyme inhibitors increase the risk of myopathy when used with such statins. Examples of those enzyme inhibitors are: erytheromycin, azole antifungals, cimetedine, methotrexate, cyclosporin, gemfibrozil, verapamil and amiodarone.
   

• Indications:

1. Secondary prevention of coronary heart disease and cerebrovascular disease.
2. Treatment of some dyslipidemias such as:

- primary hypercholesterolemia
- mixed dyslipidemias
- homozygous familial hypercholesterolemia
- selected cases of heterozygous familial hypercholesterolemia

• Contraindications:

1. Pregnancy and lactation: statins should not be given even to those women planning to get pregnant (statins should be stopped 6 months before getting pregnant).
2. Active liver disease.
3. Mypathies.

• The following table summarizes the dosing of different statins:

Click on table to view

Mitral valve . . . Where did this name come from?

Have you asked yourself this question. Why the left atrioventricular valve (or the bicuspid valve as some old books say) is commonly known as the mitral valve. In fact the name mitral is now the most commonly use name and it may sound strange somewhat if you use any either of the other 2 forementioned names. Then what does mitral mean. The word "mitre" is used to name the hat worn by catholic bishops and cardinals in ceremonies. Here is some mitre.

When you turn the open mitral valve upsidedown you will find it looking like the mitre. They say a picture worth 1000 word, so let us save the words. Here is the piture.

Lipoprotein Metabolism

Lipoprotein Metabolism

Basic definitions and terms:

- Lipoproteins: complex compounds formed of lipids bound to proteins to facilitate the transfer of lipids between different tissues.

- Apoproptein: (also called apolipoprotein) the protein ingredient of lipoproteins.

- Integral protein: it is an essential component protein which is penetrating through the whole thickness of the phospholipid layer of lipoprotein particle. Examples: apoA, apoB100 and apoB48.

- Peripheral protein: surface protein component of the lipoprotein which can be exchanged between different types of lipoproteins and act as enzyme activator or receptor binding site.

- Centrifugal transport: transport of lipids from liver to the peripheral tissues, e.g. adipose tissue and muscles.

- Centripetal transport: transport of lipids from peripheral tissues to the liver.

Chylimicrons:

• Synthesis: in the epithelial cells of the small intestines (enterocytes)

- The lipid component is synthesized from the absorbed dietary fatty acids, monoacyl glycerol and cholesterol.

- The apolipoprotein part (apoB48 and apoA) is synthesized in the rough endoplasmic reticulum by the ribosomes.

- The assembly of lipids with apolipoproteins takes place in the Glogi apparatus then they are packed into secretory vesicles where they are secreted by exocytosis into the intercellular space.

- The chylimicrons in this form are called nascent and are drained into the lacteals. They reach the thoracic duct and enter the venous circulation where they receive apoC and apoE from HDL to become mature chylimicrons.

• Structure: mature chylimicrons are about 1µ in diameter and consist of 2% proteins (apoB48, apoA. apoC and apoE) and 98% lipids (mainly triglycerides).
• Fate: the mature chylimicrons reach the peripheral tissues (adipose tissue and skeletal and cardiac muscles) where they are acted upon by the enzyme plasma lipoprotein lipase (LPL) which needs apoCII for its activation. This enzyme is present anchored with heparin sulfate to the capillary endothelium of the fore mentioned tissues. The action of this enzyme results in hydrolysis of triglycerides into glycerol and free fatty acids. The fatty acids are taken up by the cells in these tissues and are either used in the production of energy (skeletal and cardiac muscles) or used in the synthesis of tissue or milk fat (adipose tissues and lactating mammary glands. After losing the main bulk of its triglycerides, the chylimicrons returns the apoA and apoC back to the HDL and become chylimicron remnants. These particles give most of the remaining triglycerides to the HDL in exchange for cholesterol esters by means of CETP (cholestryl ester exchange protein also known as apoD). Then they are recognized by the liver through their apoE component and become endocytosed by the liver cells where they are hydrolyzed into amino acids, cholesterol and fatty acids.
• Function: transport of the absorbed dietary (exogenous) triglycerides to the tissues. They also transport dietary cholesterol and fat soluble vitamins to the liver.

N.B's:

- Plasma lipoprotein lipase is called clearing factor because it clears the plasma from its turbidity caused by the presence of chylimicrons.

- Plasma lipoprotein lipase is activated by insulin and heparin.

- The chylimicrons are called so because they are 1µ in diameter and present in lymph (chyle).

- ApoB48 is encoded by the same gene for apoB100 with the addition of termination code to the mRNA by RNA editing enzymes. It has 48% of the molecular weight of apoB100.

- The neonatal liver has the enzyme LPL.

- Normally chylimicrons can not be detected in the plasma in the fasting state (>12 hours after meals).

Very low density lipoproteins (VLDL):

• Synthesis: in the liver cells (hepatocytes)

- The triglyceride component is synthesized de novo or by re-esterification of free fatty acids.

- The apolipoprotein (apoB100) is synthesized in the microsomes.

- The VLDL in this form is called nascent and is secreted into the sinusoids. They venous circulation where they receive apoC and apoE from HDL to become mature VLDL.

• Structure: VLDL consists of 10% proteins (apoB100, apoC and apoE) and 90% lipids (mainly triglycerides).
• Fate: the mature VLDL reaches the peripheral tissues (adipose tissue and skeletal and cardiac muscles) where it is acted upon by the enzyme plasma lipoprotein lipase (LPL) which needs apoCII for its activation. The action of this enzyme results in hydrolysis of triglycerides into glycerol and free fatty acids. The fatty acids are taken up by the cells in these tissues and are either used in the production of energy (skeletal and cardiac muscles) or used in the synthesis of tissue or milk fat (adipose tissues and lactating mammary glands. After losing the main bulk of its triglycerides, the VLDL returns the apoC back to the HDL and become VLDL remnants (IDL). These particles give most of the remaining triglycerides to the HDL in exchange for cholesterol esters by means of CETP (cholestryl ester exchange protein also known as apoD). Then VLDL remnants give their apoE back to the HDL and become LDL.
• Function: centrifugal transport or the endogenous triglycerides.

Low density lipoproteins (LDL):

• Synthesis: LDL is formed of IDL (VLDL remnants) after exchange of triglycerides for cholesterol ester with HDL and loss of apoE.
• Structure: LDL consists of 20% proteins (apoB100) and 80% lipids (mainly cholesterol).
• Fate: the LDL binds to specific LDL receptors in the liver and peripheral tissues, then it is uptaken and hydrolyzed to give cholesterol.
• Function: important source of cholesterol for peripheral tissues.

High density lipoproteins (HDL):

• Synthesis: HDL is synthesized in the cells of liver and small intestine as discoidal HDL.
• Structure: HDL consists of 32-55% proteins (apoA, apoC, apoE and apoD) and 45-68% lipids (phospholipids and cholesterol).
• Fate: the HDL receives free cholesterol from tissues. This cholesterol may get esterified with fatty acids by means of LCAT (licethine cholesterol acyl transferase). The cholesterol esters are stored between the phospholipid bilayer transforming discoidal HDL to spheroidal HDL. Later on cholesterol esters may be given to chylimicron remnants or VLDL remnants in exchange for triglycerides by means of apoD (CETP cholesterol ester transfer protein).
• Function: - centripetal transport of cholesterol (reverse cholesterol transport pathway).

- reservoir for apoE and apoC needed for maturation of chylimicrons and VLDL.

Pathology of cardiomyopathy

While I am preparing for my master degree exam - 1st part, I noticed the topic of cardiomyopathy is much frequently encountered in pathology exams. I also noticed that our Egyptian pathology books are very deficient when dealing with this important topic. So, I decided to write it myself collecting data from different Pathology texts. It was "Robin's basic pathology, 8th ed" which I found most informative and well-organized and most of data here are derived from it.

Cardiomyopathy

Definition

Group of diseases that primarily involve the myocardium and produce myocardial dysfunction (or intrinsic disease of the cardiac muscle)

Types of cardiomyopathy

1. Dilated (congestive)

2. Hypertrophic

3. Restrictive

click image to enlarge

Dilated cardiomyopathy

1. Epidemiology
1. Incidence: Most common cardiomyopathy (90% of cases)

The incidence of this disorder in Europe and North America is 2-8 cases per 100 000 per year. The median age at presentation is about 50 years but young adults may be affected.

2. Etiology:
1. Idiopathic (most common)
2. Genetic causes (25-35%)
3. Myocarditis (usually postviral myocarditis with coxsackievirus B)
4. Toxic: e.g., doxorubicin(adriamycin), cocaine and cobalt.
5. Postpartum state
6. Alcoholism:can cause thiamine deficiency in addition to the acetaldehyde (alcohol metabolite) which is toxic to the myocardium.
1. Pathophysiology
1. Decreased contractility with a decreased EF (<40%)>
2. Systolic dysfunction type of left ventricular failure
   
2. Gross picture:
1. Global enlargement of the heart (the heart is 2-3 times the normal size and flobby)
1. All chambers are dilated.
2. Echocardiography shows poor contractility and mural thrombi may be present.
3. No significant 1ry valvular disease (except for functional regurgitation 2ry to ventricular chamber enlargement)
4. No significant affection of the coronary arteries.
3. Microscopic picture:

The histologic abnormalities in DCM are nonspecific. Microscopically most myocytes are hypertrophied with enlarged nuclei, but many are attenuated, stretched, and irregular. There is variable interstitial and endocardial fibrosis; scattered scars are also often present, probably marking previous myocyte ischemic necrosis caused by reduced perfusion (due to poor contractile function) and increased demand (due to myocyte hypertrophy). The extent of the changes frequently does not reflect the degree of dysfunction or the patient's prognosis.

5. Complications:
1. Biventricular CHF
2. Bundle branch blocks
3. Atrial and ventricular arrhythmias
4. Mural thrombi and systemic embolisation
6. Prognosis: poor and only 50-60% of patients survive 2 years after presentation.

click image to enlarge

Hypertrophic cardiomyopathy

1. Epidemiology
1. Most common cause of sudden death in young individuals
2. Familial form (autosomal dominant) in young individuals (majority of cases)
• Due to mutations in heavy chain of β-myosin and in the troponins
3. Sporadic form in elderly people
2. Pathophysiology
1. Hypertrophy of the myocardium
• Disproportionately greater thickening of the interventricular septum than of the free left ventricular wall
2. Obstruction of blood flow is below the aortic valve
• Anterior leaflet of the mitral valve is drawn against the asymmetrically hypertrophied septum as blood exits the left ventricle.
3. Aberrant myofibers and conduction system in the interventricular septum
• Conduction disturbances are responsible for sudden death.
4. Decreased diastolic filling: Muscle thickening restricts filling.
3. Gross picture:

- massive myocardial hypertrophy without ventricular dilation

- disproportionate thickening of the ventricular septum relative to the left ventricle free wall

- On longitudinal sectioning, the ventricular cavity loses its usual round-to-ovoid shape and is compressed into a "banana-like" configuration

- an endocardial plaque in the left ventricular outflow tract is often present with thickening of the anterior mitral leaflet. This is correlated to contact between the anterior mitral valve leaflet and the septum during late systole (dynamic obstruction)

4. Microscopic picture:

- severe myocyte hypertrophy

- myocyte (and myofiber) disarray

- interstitial and replacement fibrosis

5. Complications and Prognosis:
1. Heart failure: due to impaired diastolic filling and dynamic outflow tract obstruction (in 25% of cases).
2. Arrythmias: atrial and ventricular arrhythmias and heart block.
3. Infective endocarditis of the mitral valve.
4. Sudden cardiac death: the most common cause of SCD in young adults.

click image to enlarge

Restrictive cardiomyopathy

1. Etiology
1. Tropical endomyocardial fibrosis: the most common cause worldwide
2. Infiltrative diseases
• Examples-Pompe's glycogenosis, amyloidosis, hemochromatosis
3. Endocardial fibroelastosis in a child (thick fibroelastic tissue in the endocardium), sarcoidosis
2. Pathophysiology

a. Decreased ventricular compliance

b. Usually secondary to infiltrative disease of the myocardium

c. Diastolic dysfunction type of LHF

3. Gross picture:

- The ventricles are of approximately normal size or slightly enlarged, the cavities are not dilated, and the myocardium is firm.

- Biatrial dilation is commonly observed.

4. Microscopic picture:

- interstitial fibrosis, varying from minimal and patchy to extensive and diffuse

- disease-specific features can be seen on endomyocardial biopsy (e.g., amyloid, iron overload, sarcoid granulomas).

5. Prognosis and complications: CHF and Arrhythmias (conduction defects)

Swanton's Cardiology

This is a really good book for cardiology. I recommend it to all fellows.


Swanton's Cardiology
By R. Howard Swanton, Shrilla Banerjee

• Publisher: Wiley-Blackwell
• Number Of Pages: 696
• Publication Date: 2008-04-11
• ISBN-10 / ASIN: 1405178191
• ISBN-13 / EAN: 9781405178198

You can download it from here:

Download link

Back to basics: ECG criteria of atrial enlargement

Righ Atrial Enlargement (RAE):

• In lead II: Peaked P wave (A-like appearance)
• Normal P-wave duration
• Increase in the maximal amplitude of the P wave to >0.20 mV in leads II and aVF, and to >0.10 mV in leads V1 and V2

Left Atrial Enlargement (LAE):

• In lead II: gives a notch in the P-wave followed by a second hump (M-like appearance)
• Prolonged P-wave duration(>0.12s) and prollongation of the negative terminal portion of P-wave in lead V1
• Increase only in the amplitude of the terminal negatively directed portion of the P-wave in lead V1 to >0.10 mV

ECGs of patients with atrial enlargement. Arrows, P-wave changes in atrial enlargement; asterisks, left-atrial enlargement.(click image to enlarge)

Good book: ACLS Review: Pearls of Wisdom

ACLS Review: Pearls of Wisdom



A very nice book that will help you to master all knowledge needed for ACLS in almost every possible situation. It is in the form of Q&A which makes it more interesting. You can download the 6mb pdf document from either links below.



link 1



link2

New guidelines for appropriateness for coronary revascularization

These are the recently released guidelines to help in decision making regarding coronary revascularization. They ilustrate 180 possible scenarios and help with appropriate decision in each. you can download the pdf file from here:

http://content.onlinejacc.org/cgi/reprint/j.jacc.2008.10.005v1.pdf.

And do not forget to get your CME credit from medscape here:

http://www.medscape.com/viewarticle/586383

Echocardiography Basics explained by video

Here is a basic echocardiography course presented by some Indian university as a part of postgraduate diploma on cardiology. The resolution is not so good but acceptable. The videos is a very good start as I think.
part 1

part 2

part 3

part4

The way you think about COPD may change after you read this

Here is an interesting article about the relation between COPD and cardiovascular risks. I think it may change your way of thinking when you dealing with COPD patients either with associated cardiovascular disease or not.

Impact of Cancers and Cardiovascular Diseases in Chronic Obstructive Pulmonary Disease CME