New Classification of Ischemic Heart Disease( IHD)

The  definitions of disease have been updated about once every five years, so a revision this year would be timely. Presumably, new definitions will separate out at least some MINOCA.

What is the origin of these new terms: myocardial infarction with non-obstructive coronary arteries (MINOCA) and ischemia and no obstructive coronary artery disease (INOCA)?

It has been common for cardiologists to describe patients with chest pain and abnormal stress tests, but mild or no CAD on catheterization, as “false positives.” However, studies have long shown that such patients have a worse prognosis than patients with normal stress tests. In recognition of this fact, these patients have now been designated as “INOCA.”

 MINOCA patients have been particularly common with the advent of sensitive troponin testing. For the most part, cardiologists have done reasonably well in identifying the causes of the troponin elevations, though many cases have remained troubling, and some have still been written off as false positives. The term itself was coined in 2013.

It often applies to type 2 MI. What are the causes of MINOCA and INOCA? Generally speaking, INOCA is associated with conventional cardiac risk factors such as hypertension, hyperlipidemia, and obesity. It is much more common in women. Underlying mechanisms may involve decreased coronary flow reserve and elevated platelet reactivity. Coronary intravascular ultrasound can reveal more extensive atherosclerosis than is appreciated on angiography, due to positive remodeling. This may indicate a diffuse inflammatory state in the vessels.

 MINOCA encompasses a heterogeneous group of issues, including: Plaque rupture without severe obstruction, but with resultant vasospasm, microscopic thromboembolism, or thrombosis with spontaneous thrombolysis. Technically a type 1 MI Vasospasm without plaque rupture Thromboembolism due to thrombophilic state Coronary dissection, if not visible on angiography Takotsubo (stress) cardiomyopathy Type 2 MI with other primary diagnosis (e.g. sepsis, hypertensive crisis, arrhythmia, severe valvular disease) Pulmonary embolism and myocarditis can cause this picture, but are not considered to produce myocardial infarction. In this context, what do coders and clinical documentation integrity specialists need to know about MINOCA and INOCA – and when? These diagnoses only come into consideration after cardiac catheterization (and perhaps infrequently after coronary CT) since they require objective evidence of non-obstructive CAD. Thus, catheterizations that do not result in percutaneous intervention or CABG should be scrutinized.

برای مطالعه این مقاله بزبان فارسی -لطفاً اینجا کلیک نمایید ...

ESC 2017th guidelines updates on STEMI

The following are key points to remember about the 2017 European Society of Cardiology (ESC) Guidelines for the Management of Acute Myocardial Infarction in Patients Presenting With ST-Segment Elevation:

1. Despite the decline in acute and long-term death associated with ST-segment elevation myocardial infarction (STEMI), in parallel with the widespread use of reperfusion, mortality remains substantial. The in-hospital mortality rates of unselected patients with STEMI in national European registries vary between 4–12%.
   
2. Women tend to receive reperfusion therapy and other evidence-based treatments less frequently and/or in a delayed way than men. It is important to highlight that women and men receive equal benefit from a reperfusion and other STEMI-related therapies, and so both genders must be managed equally.
    
3. In some cases, patients may have coronary artery occlusion/global ischemia in the absence of characteristic ST-elevation (e.g., bundle branch block, ventricular pacing, hyperacute T waves, isolated ST-depression in anterior leads, and/or universal ST-depression with ST-elevation in aVR). In patients with the mentioned electrocardiographic (ECG) changes and clinical presentation compatible with ongoing myocardial ischemia, a primary percutaneous coronary intervention (PCI) strategy (i.e., urgent angiography and PCI if indicated) should be followed. 
   
4. STEMI patients should undergo a primary PCI strategy unless the anticipated absolute time from STEMI diagnosis to PCI-mediated reperfusion is >120 minutes, when fibrinolysis should be initiated immediately (i.e., within 10 minutes of STEMI diagnosis).
    
5. Patients with ST-elevation on post-resuscitation ECG should undergo a primary PCI strategy. In cases without ST-segment elevation on post-resuscitation ECG, but with a high suspicion of ongoing myocardial ischemia, urgent angiography should be done within 2 hours after a quick evaluation to exclude noncoronary causes. In all cases, the decision to perform urgent coronary angiography should take into account factors associated with poor neurological outcome. 
   
6. Routine radial access and routine drug-eluting stent implant is the standard of care during primary PCI. Routine thrombus aspiration or deferred stenting are contraindicated. 
   
7. Treatment of severe stenosis (evaluated either by angiography or fractional flow reserve) should be considered before hospital discharge (either immediately during the index PCI or staged at a later time). In cardiogenic shock, non–infarct-related artery PCI should be considered during the index procedure. 
   
8. Patients taking oral anticoagulants with renal insufficiency and/or the elderly represent a challenge in terms of optimal antithrombotic therapy. Special attention should be paid to dose adjustment of some pharmacological strategies in these subsets.
   
   
9. A sizeable proportion of STEMI patients do not present significant coronary artery stenosis on urgent angiography. It is important to perform additional diagnostic tests in these patients to identify the etiology and tailor appropriate therapy, which may be different from typical STEMI.
   
10. In some cases, there is a gap between optimal guideline-based treatment and actual care of STEMI patients. In order to reduce this gap, it is important to measure established quality indicators to audit practice and improve outcomes in real life. The use of well-defined and validated quality indicators to measure and improve STEMI care is recommended.

AHA Presidential Advisory on Dietary Fats and CVD

Cardiovascular disease is the leading cause of death world-wide. Efforts to prevent cardiovascular disease can have a major impact on global cardiovascular disease mortality. This presidential advisory from the American Heart Association reviewed the scientific evidence of multiple studies regarding the impact of dietary saturated fat on cardiovascular disease. It strongly concludes that reducing dietary intake of saturated fat and replacing it with unsaturated fat, especially polyunsaturated fat, will reduce the rate of cardiovascular disease. The following are key points to remembers. 

1-      Multiple randomized clinical trials, meta-analyses, prospective observational studies, and animal studies all support the concept of replacement of dietary saturated fats with unsaturated fats to reduce cardiovascular disease. Reducing dietary saturated fat and replacing it with polyunsaturated vegetable oil reduced cardiovascular disease by around 30%. Similar to results from statin therapy. Prospective observational studies showed that reducing saturated fat and replacing it with polyunsaturated or monounsaturated fat caused 25% and 15% reductions in coronary heart disease (CHD), respectively. Mortality overall and from other causes was also reduced.
2-      Replacing dietary saturated fats with carbohydrates, especially refined carbohydrates, does not reduce cardiovascular disease, Substitution with refined carbohydrates causes a 1% increase in CHD; substitution with whole grain carbohydrates caused a 9% reduction.
3-      Both polyunsaturated fats and monounsaturated fats are effective in reducing cardiovascular disease. The effect is greatest for polyunsaturated fats.
4-      Studies in which saturated fats were replaced by carbohydras resulting in a low-fat diet did not reduce cardiovascular disease.
5-      Animal studies have shown that a diet high in saturated fats raises low-density lipoprotein (LDL) cholesterol and increase coronary atherosclerosis, and a diet low in saturated fat but high in polyunsaturated fat has the reverse effect.
6-      Replacement of saturated fat with polyunsaturated fat, monounsaturated fat, or carbohydrates results in a reduction on LDL cholesterol; the reduction is greatest for polyunsaturated fats and least for carbohydrates.
7-      Coconut oil increases LDL without known beneficial effects. Diary fat increases LDL; substitution by polyunsaturated fats causes a 24-25% lower risk of cardiovascular disease and stroke. Trans-unsaturated fats increase cardiovascular disease. Omega-3 vegetable oil is associated with a lower risk of fatal but not overall CHD, possibly due to antiarrhythmic properties.
8-      Randomized clinical trials of a Mediterranean diets in conjunction with substitution of polyunsaturated or monounsaturated fats for saturated fats resulted in significantly reduced cardiovascular disease in the intervention arms but not in controls groups assigned to a low-fat diet.
The American heart Association Presidential Advisory strongly concedes that reducing dietary intake of saturated fat and replacing it with unsaturated fat, especially polyunsaturated fat. Will reduce cardiovascular disease incidence. Reduction in total fat i.e.; a low fat diet) is not recommended. This dietary shift should occur concurrently with the adoption of an overall healthy diet such as the Dietary Approaches to stop Hypertension diet or mideterranead diet. 

 

FFR Accuracy, Prognostic Implications, and Limitations

The Following are key points to remember about the accuracy, prognostic implications and limitations of fractional flow reserve ( FFR) :

1-    FFR is an invasive procedure used during coronary angiography to determine the functional significance of coronary stenosis.
2-      Overall, FFR is a useful adjunct to coronary angiography that allows precise quantification of the degree of myocardial ischemia.
3-      0 Its use is particularly helpful in intermediate or angiographically ambiguous lesions in the absence of noninvasive functional studies.
4-      Randomized clinical trials have demonstrated improved clinical outcomes with the use of FFR to guide coronary revascularization, including a reduction in cardiac death or myocardial infarction, as well as costs with an FFR-based strategy compared with a conventional angiography-based approach.
5-      Current societal guidelines provide a class IIa recommendation to perform FFR in angiographically-intermediate stenosis in the absence of stress testing, or in the presence of discordant stress test and angiographic findings.
6-      The appropriate use criteria for coronary revascularization also endorse the concept of “functional percutaneous coronary intervention” with revascularization decision on the basis of hemodynamic significance rather than anatomic lesion severity.
7-      Nevertheless, important questions about FFR testing remain, including the interpretation of the results (dichotomous vs. continuous), the need for hyperemia and the best pharmacological agent to achieve it, and technical aspects of the measurement that can lead to misinterpretation of the results.

8-      Attention to detail is critical when performing the FFR test.
9-      In particular, FFR results should be interpreted with caution in patients with microvascular dysfunction and conditions that can lead to it, left ventricular hypertrophy, severe aortic stenosis, and severely elevated right atrial pressure, as FFR can be artificially elevated leading to an underestimation of lesion severity.
10-   Newer technologies, such as computed tomography-based and angiogram-based FFR where FFR is mathematically derived from a computed tomography or invasive coronary angiogram, may reduce the need for invasive FFR measurements in the future. 

    Dr.Debabrata Mukherjee 

Aneurysmal left main coronary fistula to RA in asymptomatic Patient with normal Left Ventricular function ( Answer to the weekly case challenges ) .

Q: An asymptomatic 32 year old woman with a murmur. What is it?

A: Aneurysmal left main coronary fistula to RA in asymptomatic pt, normal LV function.

•Learning Tips:

•Coronary artery fistulae (CAF) are rare cardiac malformations. Their prevalence has been reported at 0.1% to 0.2% of patients who undergo coronary angiography.

•Coronary artery fistulae are either congenital or acquired coronary artery abnormalities, that have different anatomical appearance; with varying degree of shunting (Qp/ Qs); and associated cardiac anomalies .

•Etiologies include high cardiac output state and congestive heart failure with shunting of blood into a cardiac chamber, great vessel, or other structures, bypassing the myocardial capillary network .

•If the fistula is large, the intracoronary diastolic perfusion pressure diminishes progressively .

•The coronary vessel usually attempts to compensate by progressive enlargement of the ostia and feeding artery.

•Nevertheless, myocardium beyond the site of the fistula’s origin is at risk for ischemia, most frequently evident in association with increased myocardial oxygen demand during exercise or activity .

•Although aneurysm formation is common in patients with coronary artery fistulae, giant aneurysms have rarely been reported.

•They are often asymptomatic and small, however, but rupture of an aneurysmal fistula can be fatal.

•Moreover, a coronary steal phenomenon can occur owing to blood shunting and perfusion away from the myocardium. This phenomenon can be manifested in the patient as angina pectoris.

•With time, the coronary artery leading to the fistulous tract dilates progressively, that in turn, may progress to frank aneurysm formation, intimal ulceration, medial degeneration, intimal rupture, atherosclerotic deposition, calcification, side- branch obstruction, mural thrombosis, and, rarely, rupture.

•Treatment is recommended in the presence of symptoms, a giant aneurysm, or progressive enlargement of fistulae.

•In cases of small and easily accessible fistulae, transcatheter closure could be considered.

https://www.facebook.com/AfghanHeart1/

Silent Cerebral Infarct; associated with cardiac disease, procedures and other causes ! All in one

Please Click on image to become larger in SIZE

Is his bundle pacing (HBP) a feasible alternative to RV pacing now or to CRT in future?

Dr. Nabil Paktin

The answer is, the Time and Market will prove it, NOT the Knowledge and Scholars!

Estimated that worldwide, about 1-3 million patients die annually due to a Lack of a Pacemaker.
 - By comparison, about 30.000 persons die annually from influenza, 1.6 million people died of HIV/AIDS in 2012.
Death from bradycardia is entirely preventable.

Right ventricular RV apical pacing has been the standard practice for patients requiring permanent ventricular pacing however long term RV apical pacing has its drawbacks.

 A prolonged PR interval results in reduced left ventricular filling, abnormal filling pattern, presystolic mitral regurgitation due to delayed and ineffective closure of the mitral valve. Prolongation of the PR interval results from cardiac conduction disease but may also be a marker of advanced structural heart disease associated with atrial electrical and structural remodeling of a long-standing RV apical or septal pacing.
 Prolongation of PR interval by itself independently associated with an increased risk of AF, increased mortality and heart failure hospitalization in the general population, in patients with CAD and in patients with left ventricular dysfunction.

Isolated RV pacing activates the interventricular septum before the LV lateral wall, seen as LBBB pattern on the ECG due to propagation of the electrical wave front away from the sternum result in LV dyssynchrony and mismatched timing between chamber walls, with deleterious effects on LV function and adverse clinical outcomes. Including heart failure and mortality. RV pacing-induced cardiomyopathy rates of up to 20% with frequent RV pacing among patients with preserved EF is reported.

RV apical pacing deleterious effects are as follows:

1,Altered left ventricular electrical and mechanical activation

2, Altered ventricular function

3, Remodeling

4, Cellular disarray

For  Reading the Rest of Article , Please Click Bellow " Read More"!