Lateral infarction

A CT scan or MRI of the brain following a strokelike episode reveals a lucency (an area of luminosity) that is consistent with infarction. Later, cerebral atrophy and calcifications may be observed on brain imaging studies. The vascular territories of focal brain lesions and the prior medical history of these patients differ substantially from those of typical patients with stroke. Serial MRI studies often demonstrate lesion resolution, differentiating these lesions from typical ischemic strokes. An electroencephalogram is often performed when seizures are a concern. This is especially necessary in MELAS since patients occasionally have intractable status epilepticus as a terminal condition. Mental deterioration usually progresses after repeated episodic attacks. Psychiatric abnormalities (e.g., altered mental status, schizophrenia) may accompany the strokelike episodes. The encephalopathy may progress to... 

FIGURE 4.2 (Continued) A compliant balloon was used to perform angioplasty (c). Postangioplasty angiogram demonstrated complete recanalization of the basilar artery and its major branches (d and e). MRI performed 2 days later demonstrated only small areas of infarction in the cerebellar hemispheres (arrows—f and g) but no brainstem or occipital infarcts. 

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. 

Alteplase has proven effective in the early treatment of patients with acute myocardial infarction (i.e. those treated within 12 h after the first symptoms occur). Significantly increased rates of patient survival (as measured 1 day and 30 days after the initial event) are noted when tPA is administered in favour of streptokinase, a standard therapy (see later). tPA has thus established itself as a first-line option in the management of acute myocardial infarction. A therapeutic dose of 90-100 mg (often administered by infusion over 90 min) results in a steady-state alteplase concentration of 3-4 mg l 1 during that period. However, the product is cleared rapidly by the liver, displaying a serum half-life of approximately 3 min. As is the case for most thrombolytic agents, the most significant risk associated with tPA administration is the possible induction of severe haemorrhage. 

The levels of G-6-PDH in serum have been investigated in many patients suffering from a multiplicity of disorders (K6), without finding a significant change except in myocardial infarction (K7). In these cases, G-6-PDH activities reach their maxima later than other enzymes reported to increase following this event. The highest values were found about the sixth day after infarction (K6, K7). 

Amiodarone (11), a benzofuran derivative, was initially developed as a coronary vasodilator in the early 1960 s [11,12]. Several years later, the efficacy of the compound as an antiarrhythmic agent began to be exploited. The first clinical trials with amiodarone were reported in 1974 [13]. Amiodarone was effective in controlling the tachyarrhythmias of eleven patients with Wolff-Parkinson-White syndrome. Since that time the compound has been studied extensively [14,15]. Recently, in the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT), amiodarone was shown to reduce mortality during a mean 18 month period following myocardial infarction (13.8% deaths in placebo group vs. 2.1 % deaths in the treatment group) [16]. 

Obstacles remained as PTCA was not universally available and often associated with considerable time delay, especially in off peak hours. In the National Registry of Myocardial Infarction-2 (NRMI-2 >27,000 patients), total ischemia time (symptom onset to balloon inflation) was 3.9 h with onset to hospital arrival 1.6 h [45]. Unadjusted in-hospital mortality was higher in patients treated later. Door to balloon time > 2 h was related to in-hospital death (41-62% adjusted odds increase) and centers who treat >3 STEMIs/month had improved in-hospital mortality compared to less experienced facilities (Figs. 5.4 and 5.5). Lastly, similar to trials of unstable angina, PTCA was plagued by high restenosis rates... 

The results of several large clinical trials using the statin drugs (discussed later) show that the tested drugs decreased the risk of both primary and secondary cardiovascular events. The incidence of myocardial infarction and death from cardiovascular disease was reduced in patients with hypercholesterolemia who never had a... 

The paradigm shift in 1980 on the causation of acute myocardial infarction to acute coronary occlusion by a thrombus created the rationale for thrombolytic therapy of this common lethal disease. At that time—and for the first time-intravenous thrombolytic therapy for acute myocardial infarction in the European Cooperative Study Group trial was found to reduce mortality significantly. Later studies, with thousands of patients in each trial, provided enough statistical power for the 20% reduction in mortality to be considered statistically significant. Although the standard of care in areas with adequate facilities and experience in percutaneous coronary intervention (PCI) now favors catheterization and placement of a stent, thrombolytic therapy is still very important where PCI is not readily available. 

A 58-year-old man with a previous smoking history and a history of hypertension was severely biochemically hypothyroid (serum TSH 221 mU/1) and was given thyroxine, initially in a low dose (25 micrograms/day), increasing to 100 micrograms/day after 2 weeks. A month later he sustained a subendocardial myocardial infarction associated with only minor abnormalities on coronary angiography. 

A 71-year-old woman who had undergone total thyroidectomy with subsequent irradiation because of follicular carcinoma 3 years before (22). Since then, she had taken oral levothyroxine 0.15 mg and 0.2 mg on alternate days. When latent hypothyroidism became evident despite replacement therapy, the dose of levothyroxine was increased to 0.3 mg/day. Three weeks later, she had formed an acute posterior myocardial infarction, although she had no previous history of coronary artery disease. Subsequent coronary arteriograms revealed no evidence of disease of the major vessels. Myocardial scintigraphy 3 weeks after infarction still showed a persistent perfusion defect. 

A 55-year-old woman with a history of chronic pancreatitis developed epigastric pain and melena and was found to have a splenic artery pseudoaneurysm expanding a pseudocyst. She was given an intravenous bolus of octreotide followed by an infusion of 50 micrograms/ hour. A CT scan subsequently suggested thrombosis of the pseudoaneurysm, with segmental splenic infarction. Nine months later the pseudoaneurysm had recanalized. 

---