Coronary artery disease – The greatest threat to women’s health

We have greatly enjoye dreading the recently published article by Pathak LA et al. .

 There is an overwhelming evidence that gender disparities do exist in the risk factor profile and the management of patients with coronary artery disease (CAD).

The authors have retrospectively analyzed the clinical and angiographic profile of 3250 women undergoing coronary angiogram over a period of  6 years.

This is a large cohort and results are likely to influence the future research on the effect of various risk factors on the e development of CAD in women. However, we have few concerns:

1. The authors have not analyzed the distribution of various risk factors according to different age categories among women. It would have better reflected the differences in the risk factor profile among young and elderly women and might have provided causal implications.

2. Similarly, it would have been better to look for the differential pattern of angiographic findings across different age categories. Limited contemporary data exist on the differences in angiographic profile among young and elderly Indian women .

3. Third, we would like to bring attention towards the possible typographical errors. There are discrepancies in the data provided in the pie-charts and the text. In the pie-chart demonstrating the modes of clinical presentation, it is mentioned that unstable angina/NSTEMI was observed in 60%, STEMI in 20%, stable angina in 16% and atypical presentation in 4%. However in the text, these percentages are different (NSTEMI 51%, STEMI 13% and stable angina 25%).

 Similarly, discrepancies exist between the values mentioned in the pie-chart on angiographic profile and the supported text.

4. Lastly, the data were collected retrospectively by authors from a single center in Mumbai, India. Since the characteristics of CAD patients vary with socio-demographic profiles, and 69% of Indian population is rural , further studies are warranted across other partsofthecountrytoassess theclinical andangiographicprofiles among women.

This would help in the planning of preventive health programs against rising burden of CAD among women.

"خلاصه "
تحقيق جديد كه حتى درژورنال لانست ( The Lancet) نشر شد خيلى تكان دهنده و در عين حال بحث برانگيز است.
🔵 اين تحقيق ORBITAبه حمايت تحقيق هاى قبلى نشان ميدهد كه گذاشتن ستنت هاى رگهاى قلبى نزد گروه از بيماران مصاب بندش مزمن رگهاى قلب ( آنجين ثابت) بهتر ار تداوى دوايي نيست
.
🔵 يكى از مشكلات نزد بيماران با آنجين ثابت اينست كه با قدم زدن و فعاليت فزيكى نزد شان درد هاى قفس سينه ( صدر) پيدا ميشود و درين تحقيق نشان داده شده كه تداوى دوايى بهتر از گذاشتن ستنت ها براى كنترول اين مشكل در حين فعاليت فزيكى كمك مى كند .
🔵 اينكه ماهيت تداوى مداخلوى رگهاى قلب و گذاشتن ستنت نزد بيماران مصاب حملات قلبى از فوايد حياتى بشمار ميرود ، ولى مطابق جديد ترين گزارشها حدود ٦٪‏ از بيماران مصاب حملات قلبى در كشور هاى جنوب شرقى به مراكز تداوى مداخلوى قلب ميرسند و اكثريت بيماران بدون حملات حاد قلبى يعنى بيماران مزمن از گذاشتن ستنت مستفيد ميشوند ولى تداوى دوايى بهتر از گذاشتن ستنت نزد اين گروه بيماران گزارش ميشود .
🔵 تحقق چنين تحقيقات كه سرنوشت تجارت ستنت گذارى رگهاى قلبى را در جهان خدشه دار بسازد بدون شك نزديك است .

برای مطالعه بیشتر لینک زیر را کلیک نمایید .
For More information please click the following link. 

https://www.medscape.com/viewarticle/888011?nlid=118857_3801&src=WNL_mdplsnews_171103_mscpedit_card&uac=201909PZ&spon=2&impID=1473568&faf=1

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.

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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

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Answer to an echocardiogram case challenge of the April?

Severe primary pulmonary hypertension with secondary RVH, dilation and dysfunction. Atrial septal aneurysm. Late contrast (after > 3 beats).
Saline microbubbes in left heart within 3 beats of arrival in RA = intracardiac shunt. 
Late = transpulmonary passage

IVC Filter Implantation for prevention of recurrent Pulmonary Embolism !

Pearls about DVT and Pulmonary embolism,

-Venous thromboembolism (VTE) is a serious preventable cause of morbidity & mortality in the world. -DVT & pulmonary embolism (PE) are distinct but related aspects of VTE. Being silent (80% DVT) and difficult to diagnose it poses great challenges in establishing diagnosis.-Higher incidence, underestimation of risk, low level of clinical suspicion, under-used prophylaxis with high fatality has made DVT a world wide cause for concern. -The immediate need of the hour is to have standard guidelines for management of DVT.

MECHANISM :

Based on Virchow’s triad; development of D.V.T. is primarily related to the stasis of blood flow, vascular wall damage, activation of clotting system and hypercoaguable state.
Blood passing through the deepest veins in calf or thighs flows relatively slowly than from a solid clot which becomes wedged in the veins.

-Estimates suggest that 60,000-100,000 Americans die of DVT/PE (also called venous 10 to 30% of people will die within one month of diagnosis.

-Sudden death is the first symptom in about one-quarter (25%) of people who have a PE.

-Among people who have had a DVT, one-half will have long-term complications (post-thrombotic syndrome) such as swelling, pain, discoloration, and scaling in the affected limb.

-One-third (about 33%) of people with DVT/PE will have a recurrence within 10 years.

-Only 1/3 of the hospitalized patients with risk factors for blood clots received preventive treatment .

-Without preventive treatment, Upto 60% patients who undergo total hip replacement surgery may develop D.V.T.

-Cancer patients undergoing surgical procedures have at least two times the risk of post operative D.V.T. and greater than three times risk of fatal P.E. than non cancer patients undergoing similar procedure.

-In elderly, D.V.T. is associated with 21% one-year mortality rate and P.E. is associated with 39% one-year mortality rate.

-P.E. is the leading cause of maternal death associated with childbirths.
A woman’s risk of developing DVT is six times greater when she is pregnant.
.

-Evaluation and proper management is essential to decrease the burden of V.T.E.
-While surgical patients seem to draw attention of medical fraternity; it needs to be remembered that non-surgical medical patients are at an equal or at higher risk of developing V.T.

PREDISPOSING FACTORS :

Patient Factors :

-Age> 40 risk increase exponentially with age

-Obesity (BMI > 30 kg/ m2) 

-Varicose veins or venous thrombophlebitis

-Previous D.V.T.

-Oral contraceptives & Hormone replacement therapy ; oestrogen is responsible for D.V.T.

-Pregnancy : due to 

(i) Hormonal Changes

(ii) Pressure on veins by fetus

-Highest incidence in puerperium especially just after childbirth

-Dehydration : increase blood viscosity

Immobility : Stasis of blood

Long distance travel : due to (i) Inactivity  (ii) Dehydration

due to these factors blood becomes more sticky specially if journey is for more than 5 hrs. 
          - Blood disorders  

 

 

Myth of ST-elevation in AVR and ACS ! , If you hear hoofbeats think horses not zebras And if you see hoofbeats of ZEBRA not to thinks about any Horse !

If you find ST-elevation in AVR and ST-segment change in other leads , first see these doubts on Echo before thinking about ACS or taking into Cath Lab, if all walls contracting well then ACS is ruled out.

ST elevation in aVR is not entirely specific to LMCA occlusion.
ST Elevation in aVR may also be seen with:
-Proximal left anterior descending artery (LAD) occlusion
-Severe triple-vessel disease (3VD)
-Diffuse subendocardial ischaemia – e.g. due to O2 supply/demand mismatch,

Mechanism of ST elevation (STE) in aVR

-Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR.
-Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum. Infarction in this area could theoretically produce ST elevation in aVR.
-ST elevation is aVR is postulated to result from two possible mechanisms:

-Diffuse subendocardial ischaemia, with ST depression in the lateral leads producing reciprocal change n aVR  most likely).
Infarction of the basal septum, i.e. a STEMI involving aVR.

BUT THESE ALL ARE ECG concepts , ECHO will SHOW YOU THE ECG IN REAL LIFE .

:)

What is grave sign or “tombstone” ST segment elevation of MI ( Tombstoning ECG =grave prognosis)

Tombstoning ST elevation myocardial infarction can be described as a STEMI characterized by tombstoning ST-segment elevation. This myocardial infarction is associated with extensive myocardial damage, reduced left ventricle function, serious hospital complications and poor prognosis. Tombstoning ECG pattern is a notion beyond morphological difference and is associated with more serious clinical results.

It appears that a sudden occlusion of a coronary artery supplying a large area of unprepared myocardium; i.e. myocardium not protected by collaterals or ischemic preconditioning, results in complete transmural injury rapidly progressing to complete infarction, resulting in this characteristic ECG pattern. The extensive nature of the myocardial infarction and the resultant left ventricular damage and dysfunction may explain the higher risk of complications and mortality associated with this finding. The higher BNP levels on presentation in patients with tombstone STEMI seem to support the extensive nature of the myocardial damage associated with this ECG finding.

Recurrent Vasospastic Myocardial Infarctions and Hand Necrosis

A 30-year-old male smoker presented to the emergency department with anterior ST-segment elevation myocardial infarction. Primary percutaneous coronary intervention performed via the right radial artery showed an ostial thrombotic subocclusion of the left anterior descending artery (Figure 1A, black arrow) successfully treated with 2 drug-eluting stents under abciximab perfusion.

Two days later, the patient developed an inferior ST-segment elevation myocardial infarction and the repeated percutaneous coronary intervention via the same vascular access revealed a subocclusion of the previously normal mid–right coronary artery (Figure 1B, black arrow). Intravascular optical coherence tomography confirmed the angiographic suspicion of focal vasospasm (Figure 1C), showing a concentric narrowing without atherosclerosis, dissection, or thrombus.
After ineffective intracoronary nitroglycerin and verapamil injection, balloon angioplasty without stenting permitted the resolution of spasm and the alleviation of symptoms. Although drug tests were negative, the patient admitted occasional consumption of cocaine and methylamphetamine. He was discharged on oral calcium-channel blocker and dual antiplatelet therapy and the cardiac rehabilitation was uneventful.
Three months later he developed severe right hand ischemia due to extensive spastic and thrombotic occlusions of the forearm and finger arteries (Figure 1D, black arrows) refractory to vasodilators, fibrinolytic agents, and endovascular revascularization. Despite fasciotomy (Figure 1E), transradial amputation was required due to extensive necrosis. The vascular histology showed an intimal mononuclear infiltration. A cocaine-associated thromboangiitis obliterans was retained as final diagnosis.
As showed in our case, the cocaine-derived cardiovascular risks are present not only in the consumption period but could occur weeks or months later and should be considered as risk factors for dramatic outcomes.



Reference :
JACC: Cardiovascular Interventions
Volume 10, Issue 2, January 2017

What is Early Repolarization Syndrome ? Is it Benign or malignant ? Definition/Classification/ Risk factors

PCI versus early thrombolysis For patients with an ST elevation myocardial infarction

What is Free floating ball thrombus ( FFBT)? , A case of Moderate MS , mild MR and mildly dysfunctional LV and AF

Wood who first applied the term ball valve thrombus to this entity in year 1814, describe autopsy finding in 15 year old girl with rheumatic mitral valve stenosis and syncope.

Left atrial ball valve thrombus is an important pathology and left atrial (LA) ball thrombus is a rare disorder. It is most often associated with rheumatic mitral valve stenosis. However it has been reported without mitral stenosis also.

This phenomenon is seen in 17% of patients with severe mitral stenosis, and the risk doubles with atrial fibrillation.

 However, left atrial ball thrombi have rarely been reported in patients who have had no mitral valvular disease. A left atrial ball thrombus in non-rheumatic atrial fibrillation was first described in 1992.

The restricted mitral orifice encloses the free-floating thrombus in the LA. Ball valve thrombus in the left atrium (LA) is a spherical clot which is freely mobile and intermittently occludes the mitral valve orifice.

There is a potential for fatal systemic emboli or mitral valve orifice occlusion that may result in sudden death.

Almost all patients with a left atrial free floating ball thrombus have atrial fibrillation. Concomitant cardiac diseases besides of   mitral stenosis are post mitral valve replacement, myocardial infarction, myocarditis, hypertrophic cardiomyopathy and infective endocarditis.

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