Identifying Thin-Cap Fibroatheroma: Virtual-Histology Intravascular Ultrasound or Optical Coherence Tomography?

Studies have shown that two-thirds of all myocardial infarctions are caused by the rupture of plaques with large lipid content and necrotic core (NC), resulting in luminal thrombosis. Thin-cap fibroatheroma (TCFA) are characterized as a presence of a large lipid pool with overlying thin fibrous cap (<65 μm) and is associated with future major adverse cardiovascular events. The diagnosis requires a high spatial resolution (axial,lateral, elevation) and temporal.

Brown and colleagues conducted a study in 258 regions of interest from autopsied human hearts, with plaque composition and classification assessed by histology and compared with coregistered ex vivo VH-IVUS and OCT. Sixty-seven regions of interest were classified as fibroatheroma on histology, with 22 meeting criteria for TCFA. On VH-IVUS, plaque (10.91 ± 4.82 versus 8.42 ± 4.57 mm²; P=0.01) and necrotic core areas (1.59 ± 0.99 versus 1.03 ± 0.85 mm²; P=0.02) were increased in TCFA versus other fibroatheroma. Read more>>>>>>>>>>>>>>

Glycosaminoglycans (GAGs) in Cardiovascular Disease

One of the seminal discoveries in biology was the discovery of the structure of deoxyribonucleic acid, DNA, by James Watson, Francis Crick and Rosalind Franklin that led to the later deciphering of the genetic code by a series of exceptional researchers. Without Rosalind Franklin’s X ray crystallography workon the hydrated form of DNA, Watson and Crick would not have been able to decipher the double helix. It is this underlying structure that allows DNA to direct the transcription of RNA and later translation of the genetic code into proteins. 

In simple terms without understanding the structure, the genetic function of DNA was not evident. While the genetic code directs all protein synthesis, it is also true that in many instances understanding what genes are expressed and translated does not inform the actual final functions, the end result of protein expression and activity. The mere presence of a protein or enzyme also does not translate directly into an outcome in activity. Function is a much more complex process. Thus the genetic code can direct amino acid sequence and structure, but structure and location can also modify ultimate function. With this editorial we discuss the effects of one structural component, the glycosaminoglycans (GAGs), on the functional activities of other molecules, cells and organs. GAGs represent one of the silent engineers of cellular and tissue structures. Read more>>>>>>>>>>>>>>>>>

Giant Ascending Aortic Aneurysm Complicated by a Tracheal Compression

A 77 year old woman was admitted to the emergency department with complaints of intermittent cough, and sudden dyspnea since 5 days. There was no past history of hypertension and cardiac symptoms. There was no significant family history. On physical examination, the patient was dyspneic with cyanotic extremities, herroom air saturation was 90%, her heart rate was 96 beats per minute, and her blood pressure was 130/90 mm Hg. Chest auscultation found a precordial murmur. 

Chest X ray revealed a mediastinal widening and cardiomegaly. The electrocardiogram noted atrial fibrillation. Trans-thoracic echocardiography revealed a severely dilated ascending aorta, and compressing the heart with grade 3 aortic insufficiency, and normal left ventricular function. A thoraco-abdominal computed tomography scan was performed. It showed a huge aneurysm of the aortic root and involving the ascending aorta with the maximal diameter of 13.97 cm, intraluminal thrombus, compressing the trachea, with no visible intimal tear. Biological investigations showed no abnormalities.  Because of the huge diameter of the aneurysm and the compression of the trachea, we decided to perform emergent surgical repair without doing a coronary angiography. Read more>>>>>>>>>>>>>>>>>>>

Complications of Pharmacological Spasm Provocation Tests

As pharmacological spasm provocation tests, acetylcholine (ACh)  and ergonovine (ER) are employed in the cardiac catheterization laboratory. However, we often encounter the major and minor complications during performing these procedures. As a diagnostic tool, we should perform spasm provocation tests more safely without major complications. Multiple and proximal spasm documented by the pharmacological agents may occur a hemodynamic instability, such as shock and hypotension. Moreover, irreversible arrhythmia may be recognized. Selective spasm provocation tests such as intracoronary injection of ACh and ER is safer than the intravenous injection of ER. 

The effect time of ACh is very short and we may have the spontaneous remission of the provoked spasm. Therefore, we can perform a selective right and left coronary artery testing separately. We already reported the major complications during ACh spasm provocation tests in 2000. Serious major complications were not different from the reports with an intravenous injection of ER. Recently, we employed the sequential spasm provocation tests to document coronary spasm in the clinic. As sequential spasm provocation tests, we first perform intracoronary injection of ACh, second intracoronary administration of ER, and finally adding intracoronary injection of ACh just after ER test if we did not obtain the provoked spasm. Read more>>>>>>>>>>

Silent Crisis: Epidemic Hypertension in Rural West Africa

Systemic Arterial Hypertension (hereafter referred to as ‘hypertension’) is defined as blood pressure (BP) ≥140/90 mmHg. It is a major preventable cause of premature mortality through its association with Cardiovascular Disease (CVD) and renal disease. Hypertension-related CVD primarily includes stroke and Ischaemic Heart Disease (IHD). Isolated Systolic Hypertension (ISH) is more common in the elderly because the Diastolic Blood Pressure (DBP) plateaus in the 5th and 6th decades and, subsequently, gradually declines, unlike the Systolic BloodPressure (SBP), which continues to increase with age. 

Annually, approximately 8 million deaths worldwide are attributable to elevated SBP, accounting for about 14% of all deaths . This includes 54% and 47% of hypertension-attributable deaths due to stroke and IHD, respectively. The risk of death from such cardiovascular events (CE) increases in a ‘log-linear’ fashion for BP ≥115/75 mmHg, even in individuals with no known underlying vascular disease. For instance, the probability of dying from CE such as IHD and stroke is doubled for every 20 mmHg increase in SBP or 10 mmHg rise in DBP in middle-aged and elderly persons. Read more>>>>>>>>>>>>>>>>>