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.
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-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