200 years ago, in 1816, French physician René Laennec rolled a sheet of paper into a tube to auscultate the chest of a young female patient with suspected tuberculosis. Laennec went on to make his first stethoscope from two pieces of hollowed wood: one was placed against the physician's ear; the other, with a funnel-shaped cone at the end, was placed on the patient's chest. Little did Laennec realise the scientific maelstrom that would greet this new diagnostic instrument, and indeed the parallels that could be drawn to the introduction of handheld ultrasound into clinical practice some 200 years later.
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A 46-year old patient, with no cardiovascular risk factors, sought treatment for frequent episodes of irregular heartbeat and stabbing chest pain, accompanied by dyspnea and nausea at rest, which was directly related with lying on his right side. In one of these episodes, we documented atrial fibrillation with a rapid ventricular response, which spontaneously revertedto sinus rhythm. The only relevant background in the patient's medical history was hypothyroidism secondary to a thyroidectomy resulting from multi-nodular goitre. The patient was euthyroid, and received treatment with levothyroxine. A trans-thoracic echocardiogram revealed a large heteroechoic cyst-like mass behind the right atrium that was severely depressing this structure along with the left atrium, to a lesser degree (Figure 1). A computed tomography revealed a giant aneurysm of the right coronary artery, 8×8.8 cm in size, with a heterogeneous density. It emerged immediately adjacent to the root of the right coronary artery and displaced and compressed both atria (Figure 2). After confirming the diagnosis by coronary angiography (Figure 3), the patient underwent surgical exclusion of the aneurysm and plication of the atrium (right atriotomy). The patient has had a favorable postoperative evolution, with no relevant complications.
Source : Cardiologia
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
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 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.
