Absent Pericardium (Answer to X-ray case challenge of the week)

Chest X-ray challenge of this week ?

Diagnosis ?
A- Normal Chest-X-Ray
B-Rotate Film
C-Pectus excavatum
D-Absent Pericardium
E-None of above

Absent Pericardium

Increased LVEDP=Dyspnea

When studied hemodynamically, most patients with diastolic dysfunction have normal sized left ventricles and elevated left ventricular diastolic pressures (LVEDP) at rest when congestion is not present. This is a marker of increased stiffness. More refined hemodynamics indicate that left ventricular relaxation is slowed. Because of these changes, these patients have an inability to increase left ventricular end diastolic volume (LVEDV) without a great increase in end diastolic pressures. This inability to use the Frank-Starling mechanism of increasing LVEDV limits exercise since any increased volume markedly increases LVEDP and clinical dyspnea.

Hence a vicious cycle develops since the increased left ventricular pressure results in shortness of breath. This generates anxiety, increased sympathetic tone, an increased heart rate and possibly an arrhythmia such as atrial fibrillation. Ischemia secondary to coronary stenosis impairs relaxation further and increases LVEDP. Hypertension intensifies the impaired diastole further by enhancing concentric hypertrophy, a myocardium which is strong, but stiff. The inability to increase LVEDV compromises the ability to increase cardiac output, which, in turn, also stimulates the sympathetic and rennin angiotensin-aldosterone systems leading to volume retention and a further increase in LVEDP.

Coronary microcirculation disorder

Coronary microcirculation is not usually the object of routine imaging however, being the major determinant of vascular resistance - 80% of total resistance is due to coronary microcirculation - its dysfunction may compromise myocardial perfusion. Indeed, the coronary pre-arterioles and arterioles - i.e. the coronary arteries <500 μm in diameter, physiologically modulate coronary blood flow (CBF) in response to neural, mechanical and metabolic factors.

Aspirin before CABG does not increase bleeding risk !

Why is there a need to shift from CHADS2 score to the new evolved CHA2DS2-VASc score? Which one is better predictor of stroke risk?

The CHADS₂ scoring system is used to stratify stroke risk in patients with nonvalvular atrial fibrillation. Guidelines (Circulation 2006; ) recommend aspirin for patients with CHADS₂ scores of 0 (low risk), warfarin or aspirin for patients with scores of 1 (intermediate risk), and warfarin for patients with scores of ≥2 (high risk). CHADS₂, however, classifies many patients as intermediate risk, and clinicians struggle with committing these patients to long-term warfarin anticoagulation. In this study involving 74,000 patients with nonvalvular atrial fibrillation, Danish investigators compared CHADS₂ with a new system, CHA₂DS₂-VASc. CHA₂DS₂-VASc also classifies patients with scores of 0 as low risk, 1 as intermediate risk, and ≥2 as high risk .

Of 16,000 patients in the low-risk CHADS₂ category, 40% were categorized as intermediate risk and 22% as high risk by CHA₂DS₂-VASc. Of 24,000 patients categorized by CHADS₂ as intermediate risk, 93% were categorized as high risk by CHA₂DS₂-VASc. The 1-year event rate of hospital admission and death due to thromboembolism (e.g., stroke) per 100 person-years was 1.7, 4.8, and 12.3 for patients with low-, intermediate-, and high-risk CHADS₂ scores and 0.8, 2.0, and 8.8 for patients with low-, intermediate-, and high-risk CHA₂DS₂-VASc scores. Similar patterns were found during 5 to 10 years of follow-up. For both scoring systems and all risk categories, the estimated event rate was lower in patients treated with vitamin K antagonists (e.g., warfarin), except for patients with CHA₂DS₂-VASc scores of 0, in whom the event rate was unchanged.

Simple clinical risk score is required to help assess the risk of stroke in patients with atrial fibrillation. Atrial fibrillation increases the risk of stroke but this risk is not homogenous and depends on the presence of various stroke risk factors; hence, there isn’t one size which fits all. The older CHADS2 score which was described in 2001 includes five common stroke risk factors seen in non-warfarin arm in the historical trials. However in these trials the patients were not truly representative, because they only randomized <10% of the patients screened . Many of the stroke risk factors that we see in routine practice are not recorded properly or they are inadequately defined . hence we extended this in 2009 , including common risk factors that we see in our practice , including those seen in large observational trials . CHADS2 and CHA2DS2-VASc have 5 common risk factors, but why CHA2DS2-VASc is particularly good is because it reliably identifies patients at truly low risk of ischemic stroke; and these truly low risk are CHA2Ds2-VASc of zero in men and CHA2Ds2-VASc of one in females. These patients who are at truly low risk do not need any antithrombotic therapies. The next step is to offer anti-thrombotic therapy to those who have one or more stroke risk factors, in other words a CHA2DS2-VASc score of one in men and CHA2SS2-VASc of two in women and it really doesn’t matter whether the score 1, 2 or 8; we need to offer anti-thrombotic therapy to these patients, if we are serious about stroke prevention.

Final message

CHA₂DS₂-VASc is better than CHADS₂ at predicting which patients with nonvalvular atrial fibrillation are at high risk for thromboembolism. CHA₂DS₂-VASc also appears to be better at predicting which patients are truly at low risk. Broad use of the CHA₂DS₂-VASc scoring system could lower the number of patients treated with vitamin K antagonists who will not benefit from them and raise the number of patients treated with vitamin K antagonists who will.

The CAN-TREAT HFrEF + AF algorithm (Management of concomitant heart failure and reduced ejection fraction and atrial fibrillation)

The essence of Beta-Adrenoceptor Antagonists ( BAA) action in hypertension

The mechanism underlying the essential hypertension is complex and has not yet been completely defined, but it is evident that the activation of the SNS plays an important role in its pathogenesis.

Blockade of beta-AR interferes with the sympathetic regulation of the heart. The HR and contractility are only marginally affected by the BAA administration at rest, but it suppresses prominently the increases in HR and cardiac contractility induced by stress and/or physical exercises. The mechanism of antihypertensive effects of BAAs is like-wise unknown, even though a number of explanations have been proposed to play an essential role. They include the following effects:

-          Reduction of cardiac output

-          Central nervous system effects

-          Renin-angiotensin- aldosterone system inhibition

-          Reduction of plasma volume

-          Peripheral vascular resistance reduction

-          Improvement of vascular compliance

-          Baroreceptor resetting

-          Reduction of pressor response to exercise and stress-related catecholamines.

All these effects are possible proposition of a solution in the pursuit of finding the best treatment for the state of hypertension and its sequelae .