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It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced in the detection, management,

/pdf/acc-aha-2006-guidelines-for-the-management-of-patients-with-27qfh9fc7i.pdf

ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

The aim of this updated guideline is to provide comprehensive and timely evidence-based recommendations on the prevention of future stroke among survivors of ischemic stroke or transient ischemic attack. The guideline is addressed to all clinicians who manage secondary prevention for these patients. Evidence-based recommendations are provided for control of risk factors, intervention for vascular obstruction, antithrombotic therapy for cardioembolism, and antiplatelet therapy for noncardioembolic stroke. Recommendations are also provided for the prevention of recurrent stroke in a variety of specific circumstances, including aortic arch atherosclerosis, arterial dissection, patent foramen ovale, hyperhomocysteinemia, hypercoagulable states, antiphospholipid antibody syndrome, sickle cell disease, cerebral venous sinus thrombosis, and pregnancy. Special sections address use of antithrombotic and anticoagulation therapy after an intracranial hemorrhage and implementation of guidelines.

/pdf/guidelines-for-the-prevention-of-stroke-in-patients-with-4s66xf1dte.pdf

Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association

An overview of tissue and whole organ decellularization processes.

2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease) Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons

Left ventricular hypertrophy (LVH) is the major risk factor associated with myocardial failure. An explanation for why a presumptive adaptation such as LVH would prove pathological has been elusive. Insights into the impairment in contractility of the hypertrophied myocardium have been sought in the biochemistry of cardiac myocyte contraction. Equally compelling is a consideration of abnormalities in myocardial structure that impair organ contractile function while preserving myocyte contractility. For example, in the LVH that accompanies hypertension, the extracellular space is frequently the site of an abnormal accumulation of fibrillar collagen. This reactive and progressive interstitial and perivascular fibrosis accounts for abnormal myocardial stiffness and ultimately ventricular dysfunction and is likely a result of cardiac fibroblast growth and enhanced collagen synthesis. The disproportionate involvement of this nonmyocyte cell, however, is not a uniform accompaniment to myocyte hypertrophy and LVH, suggesting that the growth of myocyte and nonmyocyte cells is independent of each other. This has now been demonstrated in in vivo studies of experimental hypertension in which the abnormal fibrous tissue response was found in the hypertensive, hypertrophied left ventricle as well as in the normotensive, nonhypertrophied right ventricle. These findings further suggest that a circulating substance that gained access to the common coronary circulation of the ventricles was involved. This hypothesis has been tested in various animal models in which plasma concentrations of angiotensin II and aldosterone were varied. Based on morphometric and morphological findings, it can be concluded that arterial hypertension (i.e., an elevation in coronary perfusion pressure) together with elevated circulating aldosterone are associated with cardiac fibroblast involvement and the resultant heterogeneity in tissue structure. Nonmyocyte cells of the cardiac interstitium represent an important determinant of pathological LVH. The mechanisms that invoke short- (e.g., collagen metabolism) and long-term (e.g., mitosis) responses of cardiac fibroblasts require further investigation and integration of in vitro with in vivo studies. The stage is set, however, to prevent pathological LVH resulting from myocardial fibrosis as well as to reverse it.

Pathological hypertrophy and cardiac interstitium. Fibrosis and renin-angiotensin-aldosterone system.

Collagen plays a major role in the structural organization of the heart and therefore direct visualization of collagen fibers is a crucial component of cardiac analysis. Although linearly polarized light has proven an effective tool for the examination of myocardial collagen in histologic sections, the use of circularly polarized light may offer advantages and additional possibilities. We examined the potential enhancement of collagen analysis using circularly polarized light in two ways. We first measured the brightness, and hence indirectly assessed the birefringence, of collagen fibers in scars examined at different times after myocardial infarction. Secondly, we measured collagen content in myocardial tissue and compared results obtained from brightfield analysis of trichrome stained sections with those obtained from circularly polarized light analysis of picrosirius red stained sections. We observed a progressive increase in the maximum brightness of collagen fibers in the scar with time, and a time-dependent shift in the relative distribution of collagen fiber brightness from lower to higher levels. We found consistently lower values of collagen content in trichrome stained versus picrosirius red stained tissue, and concluded that trichrome staining underestimated collagen content. The information provided by these studies could not be obtained by brightfield analysis and could be only partially obtained from linearly polarized light analysis. Thus, analysis using circularly polarized light has the ability to enhance histologic assessment of tissue and can provide additional insights into the composition and structure of myocardial collagen.

Quantitative assessment of myocardial collagen with picrosirius red staining and circularly polarized light.

Echocardiography demonstrates prolapse of the mitral valve in at least 5 per cent of the population. Since some observations have linked this condition to stroke, we studied its incidence in two groups of patients with cerebral ischemia. The older group contained 141 patients over 45 years of age (mean, 64.7 years) who had transient ischemia or partial stroke. Prolapse was found in eight (5.7 per cent) of these patients and in 10 (7.1 per cent) of 141 age-matched controls. The second group contained 60 patients who had transient ischemia or partial stroke and were under 45 years old (mean 33.9 years). Prolapse was detected in 24 patients (40 per cent) but in only five (6.8 per cent) of 60 age-matched controls (mean age, 33.7 years). The odds ratio, 9.33, was highly significant (P<0.001). In six of the 24 patients there were other potential causes for cerebral ischemia, leaving 18 in whom the only recognizable potential cause was a prolapsing mitral valve (odds ratio, 7.00; P<0.001). This study su...

Further Evidence Relating Mitral-Valve Prolapse to Cerebral Ischemic Events

• Twelve patients who had no evidence of arteriosclerotic cerebral vascular disease, lacked hypertension or coagulation defect, and had not been receiving contraceptive therapy had recurrent transient cerebral ischemic attacks (TIAs) and partial nonprogressive strokes. All had prolapsing mitral valve proved by angiocardiography. The average age was 38 years, compared with 62 years in a larger series of patients with TIA associated with arteriosclerosis. We propose that the ischemic events are related to emboli emanating from the abnormal mitral valve with or without an associated paroxysmal cardiac arrhythmia.

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=neur&articleId=575036&pdfFileName=archneur_33_11_008.pdf

Cerebral ischemic events associated with prolapsing mitral valve.

BACKGROUNDWe sought to determine if damage to the myocardial collagen network was the cause of infarct expansion.METHODS AND RESULTSUsing polarized light microscopy, we examined sections from rat hearts obtained at 1, 2, 3, and 4 days after permanent coronary artery occlusion. Three features of the collagen network likely to be important in resisting infarct expansion were assessed: collagen quality, collagen quantity, and collagen organization. We observed a decrease in the number of normally birefringent collagen fibers in the infarct as early as 1 day after infarction. This decrease correlated significantly with time (r = -0.989, p less than 0.001). In addition, we found that the fewer normally birefringent collagen fibers present, the greater the degree of infarct expansion (assessed by measurement of total left ventricular cross-sectional area). At 4 days after infarction, we noted a loss of intermyocyte collagen struts and loss of interstitial space. These changes coincided with the onset of pronoun...

Role of collagen in acute myocardial infarct expansion.

One hundred and eighty-four consecutive patients admitted to an Investigative Stroke Unit with transient ischemic attacks (TIA) and cerebral infarction (stroke) had 48-hour automated arrhythmia monitoring, 55 patients had additional Holter monitoring and 127 patients had 2-D echocardiography. One hundred and sixteen presented with stroke (63%) and 68 patients with TIA (37%). One hundred and twenty-two were men (66.3%) and 62 were women (33.7%), mean age 63.5 years, range 25-86. The monitoring identified twelve (6.5%) patients with significant arrhythmias undetected by history, examination and admission electrocardiogram: six with atrial fibrillation (AF), four with 2 degrees heart block type Mobitz II and one each with 3 degrees heart block and sick sinus syndrome. Two-D echocardiography showed a previously unknown potential source for cardiac emboli in 22 patients (17.3%): segmental ventricular disease in eleven, mitral valve prolapse in seven, left ventricular thrombus in six, left ventricular aneurysm in three and one each with mitral valve endocarditis and global myocardial dysfunction. Only the mitral valve findings were expected on the basis of a previous M-mode echocardiographic study carried out in our city on healthy elderly volunteers. From the clinical history and all cardiac investigations, we found 59 patients (32%) with a possible cardiac source for cerebral emboli. After cerebral angiography, 29 of these 59 patients also showed a vascular lesion in the appropriate carotid artery and we could not decide definitely which lesion was responsible for the cerebral embolus. In the remaining 30 patients (16.4%), the evidence implicated the heart as the most likely source.(ABSTRACT TRUNCATED AT 250 WORDS)

Derek R. Boughner

Papers

Quantitative assessment of myocardial collagen with picrosirius red staining and circularly polarized light.

Further Evidence Relating Mitral-Valve Prolapse to Cerebral Ischemic Events

Cerebral ischemic events associated with prolapsing mitral valve.

Role of collagen in acute myocardial infarct expansion.

Value of cardiac monitoring and echocardiography in TIA and stroke patients.