Infarction types

Tohgi, H, Abe, T, Kimura, M, Saheki, M and Takahashi, S (1996) Cerebrospinal fluid acetylcholine and choline in vascular dementia of Binswanger and multiple small infarct types as compared with Alzheimer-type dementia. J. Neural Trans. 103 1211-1220. 

Figure 5.15 The ECG pattern of apical-anterior infarction (type A-2) with important anteroseptal extension as may be seen in this example but preserving the basal area of septum (D) and anterior wall (E). The lateral extension only involves the low part (D). The lack of involvement of segment 12 and lesser involvement of segment 7 are the...

Some limitations exist in the presence of Q waves in the precordial leads with respect to knowing the real extension of the infarction. This is especially true when distinguishing between the apical-anterior infarction (type A-2) and the extensive anterior infarction (type A-3). 

Figure 5.47 Patient with complete RBBB and myocardial infarction type A-3 (extensive anterior Ml). Observe the Q wave in precordial leads and the QS morphology in VL. In CE-CMR images (A-E) show important involvement of lateral, anterior and septal walls, and even the lower part...

Type I second-degree AV block with bundle branch block (which is far less common than narrow QRS type I block) must not be automatically labeled as AV nodal. Outside of acute myocardial infarction, type I block and bundle branch block (QRS > 0.12 s) occur in the His-Purkinje system in 60-70% of the cases (10) (Fig. 10.5). In such cases exercise is likely to aggravate the degree of AV block. Yet, many still believe that type I blocks are all AV nodal and therefore basically benign. It is believed that the prognosis of infranodal type I block is as serious as that of type II block and a permanent pacemaker... 

Other nootropic agents in some stage of clinical development include nebracetam (9), nefinacetam (10), and BMY 21502 (11). Nebracetam, an aminomethyl pyrrolidinone derivative, is expected to be approved in Japan in 1994 (73). In clinical studies involving patients having cerebrovascular or senile dementia of the Alzheimer s type, clinical symptoms such as spontaneous or emotional expression were enhanced in up to 71% of cases. Long-term treatment using nebracetam in patients with cerebral infarction also afforded marked improvement in most cases with few side effects (74). A review of this compound has beenpubUshed (75). 

Several clinical trials have been conducted with streptokinase adrninistered either intravenously or by direct infusion into a catheterized coronary artery. The results from 33 randomized trials conducted between 1959 and 1984 have been examined (75), and show a significant decrease in mortaUty rate (15.4%) in enzyme-treated patients vs matched controls (19.2%). These results correlate well with an ItaUan study encompassing 11,806 patients (76), in which the overall reduction in mortaUty was 19% in the streptokinase-treated group, ie, 1.5 million units adrninistered intravenously, compared with placebo-treated controls. The trial also shows that a delay in the initiation of treatment over six hours after the onset of symptoms nullifies any benefit from this type of thrombolytic therapy. Conversely, patients treated within one hour from the onset of symptoms had a remarkable decrease in mortaUty (47%). The benefits of streptokinase therapy, especially in the latter group of patients, was stiU evident in a one-year foUow-up (77). In addition to reducing mortahty rate, there was an improvement in left ventricular function and a reduction in the size of infarction. Thus early treatment with streptokinase is essential. 

Qualitative analysis of perfusion images is usually based on two assumptions that are derived from the pathophysiologic principles discussed above. First, tissue with visibly decreased CBV is so severely ischemic that it is unlikely to survive and lies within the core of the infarct. Second, tissue with decreased CBF or prolonged MTT may be mildly or severely ischemic and may or may not be salvageable. If this tissue does not appear abnormal in another, more specific type of image (such as CBV or DWI), it represents the ischemic penumbra and may potentially be rescued by immediate therapy. 

Corticosteroids have been evaluated in several types of cerebral injury, including cerebral infarction. Corticosteroids reduce vasogenic edema, such as that associated with neoplasms, but not cytotoxic edema, the type associated with ischemic stroke. A large meta-analysis found no benefit to the use of corticosteroids in ischemic stroke (or intracerebral hemorrhage), and their use is not recommended, except to treat concomitant conditions that mandate it (e.g., COPD flare). 

Everybody suffers some intellectual and memory impairment with age. If it becomes very marked or occurs earlier in life (40+) it is known as dementia. Although it may be caused by alcoholism, cardiovascular disease such as multiple infarcts, and is often seen in the later stages of Parkinsonism, the most common cause is a neurodegenerative one, namely, Alzheimer s disease (AzD). In fact this is the primary and sole cause in over half the cases of dementia and is a contributory cause in a further quarter and the younger the patient, the more likely is the dementia to be of the Alzheimer type. 

E (1999) Type of alcoholic beverage and risk of myocardial infarction , J Cardiol,... 

One eritical factor that has been neglected in considering mechanisms of cardiac fatalities is the timeframe for various types of toxicities. For example, a majority of cocaine-related fatalities and near fatalities reported from emergency rooms are attributed to one or more types of cardiac ischemic or hypertensive episodes (Isner et al. 1986). Thus, these studies may discount the cocaine-induced arrhythmias and conduction defects as important direct causes of fatalities. Yet, if coroner reports are used as data sources (Virmani et al. 1988 Wetli and Wright 1979 Mittleman and Wetli 1984), there are great numbers of deaths in which pulmonary effusion and lack of evidence for coronary occlusion, acute myocardial infarction, or... 

Understand the types of cerebrovascular disease including transient ischemic attack, cerebral infarction, and cerebral hemorrhage. 

Magnetic resonance imaging (MRI) of the head will reveal areas of ischemia earlier and with better resolution than a CT scan. Some types of imaging can reveal an evolving infarct within minutes. 

Father with a history of type 2 diabetes mellitus, hypertension, and stage 5 chronic kidney disease he died from a myocardial infarction at age 68 mother with a history of hypertension she died from injuries sustained in a motor vehicle accident at the age of 52... 

Father had type 2 diabetes and died of myocardial infarction at the age of 50 years mother is alive at 75 with no major illnesses... 

Acute coronary syndromes Ischemic chest discomfort at rest, most often accompanied by ST-segment elevation, ST-segment depression, or T-wave inversion on the 12-lead electrocardiogram. Furthermore, it is caused by plaque rupture and partial or complete occlusion of the coronary artery by thrombus. Acute coronary syndromes include myocardial infarction and unstable angina. Former terms used to describe types of acute coronary syndromes include Q-wave myocardial infarction, non-Q-wave myocardial infarction, and unstable angina. 

Creatine kinase, creatine kinase myocardial band Creatine kinase (CK) enzymes are found in many isoforms, with varying concentrations depending on the type of tissue. Creatine kinase is a general term used to describe the nonspecific total release of all types of CK, including that found in skeletal muscle (MM), brain (BB) and heart (MB). CK MB is released into the blood from necrotic myocytes in response to infarction and is a useful laboratory test for diagnosing myocardial infarction. If the total CK is elevated, then the relative index (RI), or fraction of the total that is composed of CK MB, is calculated as follows RI = (CK MB/CK total) x 100. An RI greater than 2 is typically diagnostic of infarction. 

Non-ST-segment elevation A type of myocardial infarction (MI) that is limited to the subendocardial myocardium and is smaller and less extensive than an ST-segment MI. There is usually no pathologic Q-wave on the electrocardiogram in non-ST-segment elevation. 

It is important to realize, that diseases such as myocardial infarction or type 2 diabetes represent a heterogeneous group of several distinct subphenotypes definable by clinical or biochemical characteristics. Thus, contradictory findings in pharmacogenomic studies may only not be the consequence of a lack of a major isolated gene effect (of the gene variant studied) and chance findings, but also be caused by the variability in the mix of distinct clinical phenotypes hidden beneath a common characterization such as type 2 diabetes and modulated by differences in the environment between studies. 

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