Prinzmetal’s angina, also known as Prinzmetal’s variant or Prinzmetal’s vasospastic angina is characterized by angina attacks caused by spasm of the great epicardial coronary arteries. Coronary artery endothelial dysfunction plays a crucial role in the development of this vasospastic angina. The attacks of vasospastic angina can be prevented with calcium antagonists and nitrates, whereas in refractory variant angina, coronary angioplasty with stenting may help prevent further coronary spasm. In this case report, we present a 52-year-old male patient with a transient electrocardiographic recording of acute myocardial ischemia with ST-segment elevation of the diaphragmal location accompanied by a total atrioventricular block immediately after exercise testing and as a first manifestation of Prinzmetal’s angina. After regression of the symptoms and electrocardiographic changes, significant pathomorphologic changes of coronary arteries were excluded by coronary angiography. Following discharge, the patient was treated with calcium antagonists and did not show symptoms during a 4-year follow-up period.
The vasospastic diseases and chronic pain related to lower limb have been successfully treated by surgical ablation of lumbar sympathetic trunk for last 80 years. Precise knowledge of anatomy of lumbar sympathetic trunk and its adjoining structures is mandatory for safe and uncomplicated lumbar and spinal surgeries. We aim to study the detailed anatomy of entry and exit of lumbar sympathetic trunk, the number, dimensions and location of lumbar ganglia in relation to lumbar vertebra. Thorough dissection was carried out in 30 formalin embalmed cadavers available in the Department of Anatomy, Pravara Institute of Medical Sciences (PIMS), Rural Medical College (RMC), Loni, Maharashtra. A total of 238 ganglia were observed in 60 lumbar sympathetic trunks. The sympathetic trunk traversed dorsal to the crus of diaphragm in 72.6% and in 13.3% it entered dorsal to the medial arcuate ligament. The most common site of the location of lumbar ganglia was in relation to the second lumbar vertebra, sometimes extending up to the L2–L3 vertebral disc. There was a medial shift of sympathetic trunk in lumbar region and it coursed over sacral promontory to reach the pelvic region in 96% of specimens. These variations should be kept in mind in order to prevent hazardous complications like accidental avulsion of first lumbar ganglia and genitofemoral neuritis. (Folia Morphol 2013; 72, 3: 217–222)
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The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.
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