SLOW ("POOR") R WAVE PROGRESSION

The R wave height normally becomes progressively taller from leads V1 through V6. In V1 to V3, there is an R wave of low amplitude and an S wave that is larger (R/S <1); between leads V3 to V4, there is a transition to an R wave that has a greater amplitude than the S wave (R/S >1). When the R wave height does not become progressively taller from leads V1 to V3 or V4, or even remains at low amplitude across the entire precordium, slow or poor R wave progression (PRWP) is present . Several sets of criteria have been proposed to define PRWP more precisely .

There are many etiologies for PRWP:
●Lead placement
●Anteroseptal or anterior wall myocardial infarction
●Left ventricular hypertrophy
●Left anterior fascicular block
●Left bundle branch block
●Infiltrative or dilated cardiomyopathy
●Wolff-Parkinson-White patterns due to right-sided or antero-septal bypass tracts
●Chronic lung disease
●Physiologic late transition or clockwise rotation of the heart
Poor R wave progression may be more frequently seen in females. Because there are so many different causes of PRWP, this finding alone is not useful in identifying patients with a prior anterior myocardial infarction.

Flying Defibrillator

Let’s Use Drones for Good Purpose, Let’s Use Drones to save Lives.

The traffic overcrowd cannot be the  reason of delay for cardiac arrested ones any more .

This improves current emergency infrastructure services to save the life, the ultra-fast response system moving 100 kilometers per hour which increasing the survival chance from 8% to 80% .

This can bring the average ambulance response time from 10 minutes to one .

This is equipped with camera and GPS navigation system , this will be capable of carrying oxygen mask and some injections .

Myocardial bridging:Normal , Abnormal or both !

In 5-12% of patients coronary artery Courses intramyocardial instead of coursing epicardially , this congenital coronary anomaly called Myocardial Bridging..Muscle overlying the intramyocardial segment of an epicardial coronary artery, first mentioned by Reyman in 1737, is termed a myocardial bridge, and the artery coursing within the myocardium is called a tunneled artery.

It is characterized by systolic compression of the tunneled segment, which remains clinically silent in the vast majority of cases.Coronary atherosclerosis in association with myocardial bridging has primarily been studied in the LAD. The segment proximal to the bridge frequently shows atherosclerotic plaque formation, although the tunneled segment is typically spare.
Hemodynamic forces may explain atherosclerotic plaque formation at the entrance to the tunneled segment. There, the endothelium is flat, polygonal, and polymorph, indicating low shear, whereas in the tunneled segment, the endothelium has a helical, spindle-shaped orientation along the course of the segment as a sign of laminar flow and high shear. Low shear stress may induce the release of endothelial vasoactive agents such as endothelial nitric oxide synthase (eNOS), endothelin-1 (ET-1), and angiotensin-converting enzyme (ACE). Their levels were significantly higher in proximal and distal segments compared with the tunneled segment. Thus, low shear stress may contribute to atherosclerotic plaque formation proximal to the bridge, whereas high shear stress may have a protective role within the tunneled segment. In addition, an increase in local wall tension and stretch may induce endothelial injury and plaque fissuring with subsequent thrombus formation in the proximal segment,which is supported by autopsy and clinical observations.

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Blue Toe Syndrome ( Cholesterol Embolization Syndrome)

Blue toe syndrome is characterised by tissue ischaemia secondary to cholesterol crystal or atherothrombotic embolisation. It leads to the occlusion of small vessels. Cyanosis of the digits may have several etiologies ranging from trauma to connective tissue disease, however the most common cause of blue toe syndrome is atheroembolic disease or aneurysm. Embolisation occurs typically following an ulcerated atherosclerotic plaque or aneurysms located in the aorto-iliac-femoral arterial system. Embolisation can occur spontaneously or due to a variety of causes. Most often, microembolisation appears in elderly men who have undergone an angiographic procedure or vascular surgery or even anticoagulant or thrombolytic treatment .

The differential diagnosis of blue toe syndrome includes Raynaud’s (especially secondary) phenomenon. In Raynaud’s syndrome ishaemic lesions are usually more diffuse, larger areas of distal parts of different fingers (rarely toes) are involved and are affected by vasospastic disorders. The patients are usually younger and without any known atherosclerotic disease. In blue toe syndrome skin lesions are usually restricted and related to the occluded artery, fingers are rarely affected as opposed to toes and vasospasm is usually absent. Painful red, purple, blue or black toes can also be seen in patients with thrombocythemia associated with polycythemia vera or in essential thrombocythemia (3). In these patients, ischemic lesions of fingers or toes are caused by arteriolar inflammation and the thrombosis of microvessels that appear as a consequence.

 The following 6 key elements are required for the development of cholesterol embolization syndrome:

1. Presence of a plaque in a proximal, large-caliber artery (such as the internal carotid artery, the iliac arteries, or the aorta)
2. Plaque rupture (spontaneous, traumatic, or iatrogenic)
3. Embolization of plaque debris (containing cholesterol crystals, platelets, fibrin, and calcified detritus)
4. Lodging of the emboli in small to medium arteries with a diameter of 100 to 200 μm, leading to mechanical occlusion
5. Foreign-body inflammatory response to cholesterol emboli
6. End-organ damage due to a combined effect of mechanical plugging and inflammation.

Definitions of PCI Success

Percutaneous coronary intervention (PCI) success may be defined by angiographic, procedural, and clinical criteria. 

1•Angiographic success in a stented artery is a minimum stenosis diameter reduction to <20% .

2-Procedural Success
A successful PCI : should achieve angiographic success without in-hospital major clinical complications (e.g., death, myocardial infarction [MI], emergency coronary artery bypass surgery) during hospitalization. MI is often defined as the development of Q waves in addition to elevation of troponins three times the upper limit of the laboratory's normal value. Cardiac troponin T and I as measurements of myocardial necrosis are more sensitive and specific than CK-MB. Enzyme elevation in the absence of new Q waves is counted as MI, peri-procedural. There is no consensus on what level of troponin alone is clinically important enough to change major management following the interventional procedure.

3-Clinical Success •A clinically successful PCI is ananatomical and procedural success with relief of signs and/or symptoms of myocardial ischemia after recovery from the procedure. The long-term clinical success requires that the patient have persistent relief of signs and symptoms of myocardial ischemia for more than 6 months. Restenosis is the principal cause of lack of long-term clinical success when short-term clinical success has been achieved.

ACE Inhibitors Side Effect Mnemonic (CAPTOPRIL)

News and Views :Antibiotic Cotrimoxazole Combined With ACE Inhibitor or ARB Could Raise Risk of Sudden Death

October 31, 2014
TORONTO, ON — The risk of sudden death went up by more than a third in older patients taking ACE inhibitors or angiotensin-receptor blockers (ARBs) who were also put on the antibacterial agent cotrimoxazole, compared with those who were instead given amoxicillin, in a case-control study reported this week. The finding was independent of comorbidities, other medications, recent procedures, and other potential influencers of sudden-death risk, according to the authors.The elevated risk with cotrimoxazole, a combination of sulfamethoxazole and trimethoprim widely used for decades, was likely caused by its capacity for raising serum potassium, which became fatal on top of other medications known for causing hyperkalemia, speculate Dr Michael Fralick (University of Toronto, ON) and colleagues in their report, published October 30, 2014 in the BMJ. The same group had previously observed that combining cotrimoxazole with ACE inhibitors or ARBs similarly drove up the risk of hospitalization due to hyperkalemia.
"In patients who are on ACE inhibitors or ARBs, who are by definition at risk for hyperkalemia, the safest thing to do would be to use an antibiotic" other than cotrimoxazole, senior author Dr David N Juurlink (Institute for Clinical Evaluative Sciences and the University of Toronto, ON) told heartwire . "But that's not always going to be practical. Alternate strategies could be to use a lower dose or a shorter duration of the drug. Or, when you have to give trimethoprim-based antibiotics to somebody who's on an ACE inhibitor or an ARB, at a minimum being mindful of the potential for serious and even life-threatening hyperkalemia. That alone would go a long way toward reducing the dangers of this interaction."

That goes especially for some susceptible patient groups. "Patients with type 2 diabetes are sitting ducks for this," Juurlink said. "They have a tendency for hyperkalemia independent of anything else, because of what the diabetes does to their kidney function." And patients with heart failure may be on potassium-sparing spironolactone as well as ACE inhibitors or ARBs. "Someone who has reduced left ventricular function and has diabetes—there are millions of people like that in North America."
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