Akut hjärt-kärlsjukdom orsakar mer än hälften av alla dödsfall i Sverige. Många patienter med akut hjärtinfarkt uppvisar inte de klassiska symtom som vanligtvis förknippas med sjukdomen utan har en mer atypisk symtombild. Syftet med litteraturstudien var att beskriva vikten av god kunskap och kännedom om den varierande symtombild som kan förekomma vid hjärtinfarkt, sett ur ett omvårdnadsperspektiv. I metoden har 23 vetenskapliga artiklar bearbetats. Resultatet visade att förekomst av atypiska symtom var vanligare hos kvinnor, äldre och diabetiker. Män upplevde framförallt bröstsmärta, smärtutstrålning till armar och svettning. Kvinnor uppvisade bröstsmärta i mindre omfattning men upplevde däremot mer andnöd, rygg- och nacksmärta, besvär från mag-tarmkanalen, trötthet och orkeslöshet. Varningssymtom förekom hos ett stort antal patienter och framförallt hos kvinnor. Patienterna uppfattade och uttryckte sina besvär på olika sätt, vilket påverkade deras beslut att söka vård. Sjuksköterskans roll ansågs vara att informera patienter, speciellt de med högre risk att uppvisa atypiska symtom samt allmänheten om den annorlunda symtombild som kan förekomma. Sjuksköterskor måste ha god kunskap och kännedom om olikheter i symtombild hos olika patientgrupper. De bör vara lyhörda och ha en klinisk blick samt förstå vikten av god framförhållning och beredskap för ett adekvat omhändertagande. I framtiden måste kunskapen utökas och spridas bland allmänheten. Vidare forskning i ämnet är önskvärt ur ett sjuksköterskeperspektiv.

The treatment of acute myocardial infarction (AMI) has undergone a tremendous development during the last decades, and the most important factor is probably the introduction of reperfusion therapy aimed at preventing or limiting the myocardial injury. It is of vital importance that patients with AMI are adequately monitored regarding the development of ECG changes during and after treatment to identify successful or failed reperfusion and to detect episodes of recurrent ischemia. Vectorcardiography (VCG) is one method for this purpose. This series of studies was aimed at evaluating VCG as a method for detecting reperfusion and recurrent ischemia in patients with ST-elevation AMI who were treated with different reperfusion strategies. Specific changes in the VCG during the initial treatment phase, “reperfusion peaks,” were examined in detail. The influence of the fibrinolytic system and von Willebrand factor (vWF) on successful reperfusion and subsequent AMI and death after thrombolytic treatment with streptokinase (SK) was another main objective. From the data in these studies it can be concluded that: VCG is a relevant and easily used method for ischemia-monitoring in patients with AMI. A specific sign, the reperfusion peak, is associated with vectorcardiographic signs of reperfusion. This sign is observed both in patients treated with primary coronary angioplasty and in those who are treated with fibrinolytic agents. The reperfusion peak is associated with successful reperfusion and with larger infarcts, but by itself, the parameter has little prognostic significance. The recognition of the reperfusion peak is important since it can mimic severe ischemia. In an unfortunate situation the incorrect interpretation of the VCG could lead to premature treatment decisions that might even be harmful to the patient. Streptokinase treatment of patients with AMI induced profound changes in the fibrinolytic system and vWF. A high tissue plasminogen activator (tPA) activity level (>25 U/mL) early after the start of treatment, reflecting the fibrinolytic activity obtained by the given drug, was associated with successful reperfusion. Pre-existing neutralizing antibodies to SK were found to varying degrees in the previously SK-treated patients. No association between SK-neutralizing antibodies and the result of the treatment regarding successful reperfusion as judged by VCG was seen. Pre-treatment levels of tPA activity, PAI-1 activity, PAI-1 mass-concentration and vWF had no correlation with the success of reperfusion therapy with SK or on the incidence of recurrent ischemia during the first 24 hours. Recurrent ischemia, however, was shown to be an independent risk factor for death within the first 1 year. Elevated levels of PAI-1 mass-concentration, and to some extent PAI-1 activity, after the start of SK treatment, were associated with a higher risk for death at one year, though not at five years.

This thesis describes the development of new magnetic resonance imaging (MRI) methods to characterize cardiac tissue with myocardial infarction (MI). Wall motion imaging (for visualizing myocardial contraction) and viability imaging (to identify MI) are two components of cardiac tissue characterization used for prognosis and treatment planning. MRI-based wall motion and viability methods are considered the gold standard in imaging, and characterization of MRI viability images has been correlated with inducibility for ventricular tachycardia (VT). However, viability imaging with MRI has limitations such as difficulty visualizing the blood-infarct border. Wall motion and viability images are acquired separately, each requiring cardiac gating and breath holds, leading to long scan times. A novel multi-contrast delayed enhancement (MCDE) sequence was developed that simultaneously acquires wall motion and viability images. In a patient study, the MCDE sequence was demonstrated to provide improved visualization of MI compared to the conventional inversion-recovery gradient echo (IR-GRE) sequence, particularly for small infarcts adjacent to the blood pool. MCDE images also provided accurate wall motion images that could be used to calculate the left ventricular ejection fraction. An image processing algorithm was developed to analyze MCDE images to segment and classify the infarct gray zone, which is hypothesized to represent heterogeneous infarct responsible for causing VT. In a study of 15 patients with MI, the MCDE-derived gray zone was shown to be less sensitive to image noise than the IR-GRE-derived gray zone, and did not require manual contours of the blood pool which contributes to additional variability in the IR-GRE gray zone analysis. Finally, a real-time delayed enhancement (RT-DE) method was developed to provide black-blood viability images without requiring cardiac gating or breath holds. RT-DE imaging was shown to have a high sensitivity for detecting MI in a study of 23 patients. The methods described in this thesis help expand the patient population that can undergo a cardiac viability exam and help improve the visualization of myocardial infarct. Further modifications in the pulse sequences to improve the temporal and spatial resolutions are proposed with the goal of predicting and guiding treatment of ventricular tachycardia resulting from myocardial infarct.

Remote ischemic preconditioning (rIPC) through transient limb ischemia induces potent cardioprotection against ischemia reperfusion (IR) injury. I examined the delayed phase of protection that appears 24 hours after the initial rIPC stimulus. The primary objective of this study was to establish a mode of sedation and control treatment for delayed rIPC experiments. I used an ex-vivo, Langendorff isolated-mouse heart preparation of IR injury to examine the delayed effects of an intra-peritoneal (IP) injection, sodium-pentobarbital (SP), halothane and nitrous oxide (N2O) anesthesia on post-ischemic cardiac function. Each anesthetic method improved left-ventricular function after IR injury. SP and halothane anesthesia also reduced LV infarct size. Delayed cardioprotection after IP injections was associated with an increase in phosphorylated-Akt levels. The present study shows that IP injections and inhalational anesthesia invoke cardioprotection and, therefore, indicates that these modes of sedation should not be used as control treatments for studies examining the delayed rIPC phenotype.

Remote ischemic preconditioning (rIPC) through transient limb ischemia induces potent cardioprotection against ischemia reperfusion (IR) injury. I examined the delayed phase of protection that appears 24 hours after the initial rIPC stimulus. The primary objective of this study was to establish a mode of sedation and control treatment for delayed rIPC experiments. I used an ex-vivo, Langendorff isolated-mouse heart preparation of IR injury to examine the delayed effects of an intra-peritoneal (IP) injection, sodium-pentobarbital (SP), halothane and nitrous oxide (N2O) anesthesia on post-ischemic cardiac function. Each anesthetic method improved left-ventricular function after IR injury. SP and halothane anesthesia also reduced LV infarct size. Delayed cardioprotection after IP injections was associated with an increase in phosphorylated-Akt levels. The present study shows that IP injections and inhalational anesthesia invoke cardioprotection and, therefore, indicates that these modes of sedation should not be used as control treatments for studies examining the delayed rIPC phenotype.

This thesis describes the development of new magnetic resonance imaging (MRI) methods to characterize cardiac tissue with myocardial infarction (MI). Wall motion imaging (for visualizing myocardial contraction) and viability imaging (to identify MI) are two components of cardiac tissue characterization used for prognosis and treatment planning. MRI-based wall motion and viability methods are considered the gold standard in imaging, and characterization of MRI viability images has been correlated with inducibility for ventricular tachycardia (VT). However, viability imaging with MRI has limitations such as difficulty visualizing the blood-infarct border. Wall motion and viability images are acquired separately, each requiring cardiac gating and breath holds, leading to long scan times. A novel multi-contrast delayed enhancement (MCDE) sequence was developed that simultaneously acquires wall motion and viability images. In a patient study, the MCDE sequence was demonstrated to provide improved visualization of MI compared to the conventional inversion-recovery gradient echo (IR-GRE) sequence, particularly for small infarcts adjacent to the blood pool. MCDE images also provided accurate wall motion images that could be used to calculate the left ventricular ejection fraction. An image processing algorithm was developed to analyze MCDE images to segment and classify the infarct gray zone, which is hypothesized to represent heterogeneous infarct responsible for causing VT. In a study of 15 patients with MI, the MCDE-derived gray zone was shown to be less sensitive to image noise than the IR-GRE-derived gray zone, and did not require manual contours of the blood pool which contributes to additional variability in the IR-GRE gray zone analysis. Finally, a real-time delayed enhancement (RT-DE) method was developed to provide black-blood viability images without requiring cardiac gating or breath holds. RT-DE imaging was shown to have a high sensitivity for detecting MI in a study of 23 patients. The methods described in this thesis help expand the patient population that can undergo a cardiac viability exam and help improve the visualization of myocardial infarct. Further modifications in the pulse sequences to improve the temporal and spatial resolutions are proposed with the goal of predicting and guiding treatment of ventricular tachycardia resulting from myocardial infarct.

No description available.

Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 206-224).

Thesis--Columbia University. / Photocopy of typescript. Ann Arbor, Mich. : University Microfilms International, 1977. -- 21 cm. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 160-168).

Rapid restoration of blood flow to ischemic myocardium is essential, however it causes further injury called reperfusion injury. Apoptosis contributes significantly to cardiomyocyte cell death during ischemia reperfusion injury, in which caspase family proteases play an essential role as they are the executioners of apoptosis. Caspase inhibitors showed promising cardioprotective results when administered before ischemia or at the start of reperfusion. However, before applying them in pre clinical studies of myocardial ischemia, several investigations needed to be taken to determine their therapeutic window post reperfusion, their effect on functional recovery of myocardium post ischemia, their mechanism of action. Methods Isolated perfused rat hearts were subjected to 35 min ischemia followed by 2 hr reperfusion where caspase inhibitors [broad spectrum caspase inhibitor (ZVAD, 0.1µM), specific caspase 3 inhibitor (DEVD, 0.07µM)] were added at the start of reperfusion, 15, 30 and 60 min after starting reperfusion at the presence or absence of Wortmannin (WORT, 100nM, PI3-kinase inhibitor). Hearts underwent triphenyl tetrazolium staining for infarct size assessment, or were frozen for Western blot analysis. Freshly isolated adult rat ventricular myocytes were subjected to 6 hr hypoxia followed by either 18 hr, where caspase inhibitors (ZVAD, 25µM and DEVD, 25µM) were added at the start of reoxygenation, 15, 30 and 60 min after starting reoxygenation at the presence or absence of Wortmannin (WORT, 100nM). Cardiomyocytes were analysed for viability, apoptosis, necrosis and intracellular caspase-3 activity using flow cytometry analysis. Isolated adult rat ventricular papillary muscles were subjected to 35 min hypoxia followed by 100 min reperfusion where caspase inhibitors [ZVAD (0.1 µM, 2.5µM) and DEVD (2.5µM)] were added at the start of reperfusion throughout. Power output was measured using work loop technique.