Author Archives: Dr.Nabil Paktin
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.Neither nonsignificant stenosis proximal to the bridge nor systolic compression of the tunneled segment alone can sufficiently explain severe ischemia and associated symptoms. Experimental LCX occlusion, initially during systole only and then during continuing occlusion extending increasingly into diastole, resulted in distinct shortening of inflow time with significant reduction of epicardial flow, subendocardial flow, and distal coronary pressure. After releasing the occlusion, diastolic flow increased in correspondence with an increasing duration of vessel occlusion, despite a decrease in mean flow. This increased diastolic/systolic flow ratio was later verified in patients. Consistent with clinical findings, the increase in diastolic flow could not fully compensate for the decrease in mean flow resulting in reduced coronary flow reserve, which could not be explained by impaired vasodilatory capacity of resistance vessel.When arterial occlusion was limited to systole, phasic coronary blood flow and distal coronary pressure was observed to resume with considerable delay contributing to reduced myocardial oxygen consumption and increased coronary sinus lactate concentration. This delayed diastolic relaxation was later identified in humans as an important mechanism contributing to ischemia with frame-by-frame analysis of IVUS images.Angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction, myocardial stunning, paroxysmal AV blockade, as well as exercise-induced ventricular tachycardia and sudden cardiac death are accused sequelae of myocardial bridging.However, considering the prevalence of myocardial bridging, these complications are rare. Patients may present with atypical or angina-like chest pain with no consistent association between symptom severity and the length or depth of the tunneled segment or the degree of systolic compression.Resting ECGs are frequently normal; stress testing may induce nonspecific signs of ischemia, conduction disturbances, or arrhythmias.The current gold standard for diagnosing myocardial bridges is coronary angiography with the typical “milking effect” and a “step down–step up” phenomenon induced by systolic compression of the tunneled segment . However, these signs provide little information on the functional impact at the myocardial level. In the presence of a proximal stenosis, myocardial bridging may only be identifiable after PTCA when higher intravascular pressures and reversed hypokinesis unmask myocardial bridging. In patients with thin bridges, the milking effect may be missed and new imaging techniques and provocation tests may be required to detect a bridge.On the basis of the above mechanisms for ischemia, 3 treatment strategies have been explored: (1) negative inotropic and/or negative chronotropic agents, ie, β-blockers, and calcium antagonists; (2) surgical myotomy and/or CABG; and (3) stenting of the tunneled segment.References :1- Cardiosource2- Circulation3- European Society of Cardiology
4- Self- experienced data and notes
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 following 6 key elements are required for the development of cholesterol embolization syndrome:
Presence of a plaque in a proximal, large-caliber artery (such as the internal carotid artery, the iliac arteries, or the aorta)
Plaque rupture (spontaneous, traumatic, or iatrogenic)
Embolization of plaque debris (containing cholesterol crystals, platelets, fibrin, and calcified detritus)
Lodging of the emboli in small to medium arteries with a diameter of 100 to 200 μm, leading to mechanical occlusion
Foreign-body inflammatory response to cholesterol emboli
End-organ damage due to a combined effect of mechanical plugging and inflammation.
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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% .
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
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.”
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Three Types of Atrial Remodeling secondary to Atrial Fibrillation (AF) ! Difference between adaptation and Remodeling in Atrial Fibrillation (AF) .
NEWS AND VIEWS -Long-Term Outcome of PCI Versus CABG in Insulin and Non–Insulin-Treated Diabetic Patients -Results From the FREEDOM Trial
News and Views: Increased Mortality Associated With Digoxin in Contemporary Patients With Atrial Fibrillation Findings From the TREAT-AF Study
News and Views ; Atrial ﬁbrillation associated with ivabradine treatment: meta-analysis of randomised controlled trials
Objective :To quantify any risk of atrial ﬁbrillation (AF) associated with ivabradine treatment by meta-analysis of clinical trial data.
Methods Medline, Embase, Web of Knowledge and the Cochrane central register of controlled trials were searched for double-blinded randomised controlled trials of ivabradine with a minimum follow-up period of 4 weeks. For studies where AF data were unpublished, safety data were obtained from the European Medicines
Agency (EMeA) website and personal communications. Studies were appraised for risk of bias using components recommended by the Cochrane Collaboration. Metaanalyses were performed of relative risk of AF and absolute risk difference of AF per year of treatment. The main outcome measure was incident AF during the follow-up period.
AF is a substantially more common side effect of ivabradine treatment than one patient in 10 000, the risk presently reported in the product literature. The incidence of AF has not routinely been reported in clinical trials of ivabradine. Ivabradine treatment is associated with a 15% increase in the RR of AF. We estimate that 208 patient-years of treatment with ivabradine would be required to cause one new case of AF.