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PubMed1995

Redistribution of myocardial blood flow with topical nitroglycerin in patients with coronary artery disease.

BACKGROUND: Unlike nonselective coronary vasodilators, nitroglycerin (GTN) is said to exert its primary vasodilatory effect on epicardial conductance vessels. Thus, in experimental models of coronary occlusion GTN appears to preferentially direct blood flow to poststenotic zones of ischemia. This phenomenon has, to date, not been tested in humans. Using positron emission tomography we examined the effect of transdermal GTN on global and regional myocardial perfusion in patients with angiographically proven coronary artery disease. METHODS AND RESULTS: Myocardial perfusion with [13N]ammonia was estimated from dynamic time-activity curves at baseline and 3 hours following application of either a 0.4 mg/h GTN skin patch (n = 10) or a placebo patch (n = 10) in a double-blind parallel design. From resliced cross-sectional images, regional flow, expressed as [13N]ammonia retention, was estimated from 216 myocardial sectors. Ischemia was defined as a significant reduction (> 2 SDs from average counts/pixel in maximally perfused zones) in [13N]ammonia retention within 10 contiguous myocardial sectors coupled with an increase or no change in counts derived from [18F]fluorodeoxyglucose. There was no change in global myocardial blood flow as expressed by [13N]ammonia retention following either placebo (0.61 +/- 0.14 to 0.62 +/- 0.12 min-1) or GTN (0.75 +/- 0.22 to 0.74 +/- 0.19 min-1). Conversely, there was a significant increase in the proportion of blood flow to the ischemic zones with GTN (73.9 +/- 12.6% to 94.9 +/- 17.8%; P < .05). No change in the distribution of blood flow to either ischemic or nonischemic zones was observed with placebo. A slight but insignificant decrease in [13N]ammonia retention in nonischemic zones was observed with GTN (1.01 +/- 0.31 to 0.93 +/- 0.26 min-1). CONCLUSIONS: This study suggests that under resting conditions topical GTN alters myocardial perfusion by preferentially increasing flow to areas of reduced perfusion with little or no change in global myocardial perfusion in patients whose angina is responsive to GTN.

Administration, Cutaneous↗
PubMed2005

[Pathogenesis and treatment of acute coronary syndromes].

Acute coronary syndromes (ACS) include unstable angina and non-ST elevation myocardial infarction (UA/NSTEMI) and ST-segment elevation myocardial infarction (STEMI). Acute coronary syndromes lead to important epidemiological and economical problems. In polish population an estimated incidence of ACS is 250 000 cases per year. 30-day mortality in UA/NSTEMI is approximately 3.5%, and 8.4% in STEMI. The atherosclerotic plaque instability with subsequent rupture and thrombus formation is a primary mechanism of ACS. Plaque destabilization is evoked by local and systemic inflammation. The primary risk factors in ACS are: age > 65 years, diabetes, peripheral artery disease, stroke, previous myocardial infarction and elevated levels of cardiac troponins. The guidelines for treatment of ACS are based on the results of large randomized clinical trials assessing the reduction of relevant clinical end-points (death, AMI, recurrent ischaemia). The goal of treatment of UA/NSTEMI is the stabilization of the plaque, prevention and reduction of myocardial ischaemia and AMI. Inefficient medical treatment and sustained symptoms are the indication for coronary angiography and percutaneous coronary intervention (PCI). The main goal of treatment in STEMI is quick regaining of the culprit vessel patency and maintaining of sufficient myocardial perfusion. It can be done by thrombolytic therapy or primary coronary angioplasty. In comparison to fibrynolysis PCI confers the lower risk of death and recurrent AMI. New regimens of pharmacological treatment (facilitated PCI) including the half-dose of fibrynolytic and GPIIbIIIa inhibitor prior to PCI are assessed to improve the efficiency of PCI.

Acute Disease↗
PubMed1983

Sensitivity of technetium-99m-pyrophosphate scintigraphy in diagnosing cardiac amyloidosis.

To determine the value of technetium-99m-pyrophosphate myocardial scintigraphy in the diagnosis of amyloid heart disease this procedure was prospectively performed in 20 consecutive patients with biopsy-proven primary amyloidosis. Eleven patients had echocardiographic abnormalities compatible with amyloid cardiomyopathy, 9 of whom had congestive heart failure. Diffuse myocardial pyrophosphate uptake was of equal or greater intensity than that of the ribs in 9 of the 11 patients with echocardiograms suggestive of amyloidosis, but in only 2 of the 9 with normal echocardiograms, despite abnormal electrocardiograms (p less than 0.01). Increased wall thickness measured by M-mode echocardiography correlated with myocardial pyrophosphate uptake (r = 0.68, p less than 0.01). None of 10 control patients with nonamyloid, nonischemic heart disease had a strongly positive myocardial pyrophosphate uptake. Thus, myocardial technetium-99m-pyrophosphate scanning is a sensitive and specific test for the diagnosis of cardiac amyloidosis in patients with congestive heart failure of obscure origin. It does not appear to be of value for the early detection of cardiac involvement in patients with known primary amyloidosis without echocardiographic abnormalities.

Aged↗
PubMed2005

Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial.

BACKGROUND: Patients with type 2 diabetes mellitus are at increased risk of cardiovascular disease, partly owing to dyslipidaemia, which can be amenable to fibrate therapy. We designed the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study to assess the effect of fenofibrate on cardiovascular disease events in these patients. METHODS: We did a multinational, randomised controlled trial with 9795 participants aged 50-75 years, with type 2 diabetes mellitus, and not taking statin therapy at study entry. After a placebo and a fenofibrate run-in phase, we randomly assigned patients (2131 with previous cardiovascular disease and 7664 without) with a total-cholesterol concentration of 3.0-6.5 mmol/L and a total-cholesterol/HDL-cholesterol ratio of 4.0 or more or plasma triglyceride of 1.0-5.0 mmol/L to micronised fenofibrate 200 mg daily (n=4895) or matching placebo (n=4900). Our primary outcome was coronary events (coronary heart disease death or non-fatal myocardial infarction); the outcome for prespecified subgroup analyses was total cardiovascular events (the composite of cardiovascular death, myocardial infarction, stroke, and coronary and carotid revascularisation). Analysis was by intention to treat. The study was prospectively registered (number ISRCTN 64783481). FINDINGS: Vital status was confirmed on all but 22 patients. Averaged over the 5 years' study duration, similar proportions in each group discontinued study medication (10% placebo vs 11% fenofibrate) and more patients allocated placebo (17%) than fenofibrate (8%; p<0.0001) commenced other lipid treatments, predominantly statins. 5.9% (n=288) of patients on placebo and 5.2% (n=256) of those on fenofibrate had a coronary event (relative reduction of 11%; hazard ratio [HR] 0.89, 95% CI 0.75-1.05; p=0.16). This finding corresponds to a significant 24% reduction in non-fatal myocardial infarction (0.76, 0.62-0.94; p=0.010) and a non-significant increase in coronary heart disease mortality (1.19, 0.90-1.57; p=0.22). Total cardiovascular disease events were significantly reduced from 13.9% to 12.5% (0.89, 0.80-0.99; p=0.035). This finding included a 21% reduction in coronary revascularisation (0.79, 0.68-0.93; p=0.003). Total mortality was 6.6% in the placebo group and 7.3% in the fenofibrate group (p=0.18). Fenofibrate was associated with less albuminuria progression (p=0.002), and less retinopathy needing laser treatment (5.2%vs 3.6%, p=0.0003). There was a slight increase in pancreatitis (0.5%vs 0.8%, p=0.031) and pulmonary embolism (0.7%vs 1.1%, p=0.022), but no other significant adverse effects. INTERPRETATION: Fenofibrate did not significantly reduce the risk of the primary outcome of coronary events. It did reduce total cardiovascular events, mainly due to fewer non-fatal myocardial infarctions and revascularisations. The higher rate of starting statin therapy in patients allocated placebo might have masked a moderately larger treatment benefit.

Aged↗
PubMed2002

Update on aspirin in the treatment and prevention of cardiovascular disease.

Antiplatelet therapy, most notably aspirin, has been well documented to reduce risks of subsequent cardiovascular disease (CVD) in secondary prevention, acute myocardial infarction (MI), acute occlusive stroke, as well as in primary prevention. In secondary prevention, the most recent Antithrombotic Trialists' Collaboration reviewed 194 published randomized trials of antiplatelet therapy, mostly aspirin, involving more than 212 000 patients (ie, 135 000 using antiplatelet therapy or control and 77 000 using different antiplatelet regimens). In a very wide range of patients who have survived a prior occlusive vascular event-including MI, transient ischemic attacks, occlusive stroke, unstable and stable angina, percutaneous coronary interventions, and coronary artery bypass graft-aspirin prevents about 25% of serious vascular events. Among patients suffering acute Ml or acute occlusive stroke, aspirin begun promptly and continued long-term reduces risks of subsequent MI, stroke, and vascular death. In acute coronary syndromes, clopidogrel added to aspirin further reduces the risk of important vascular events, but not mortality, and causes more side effects, especially bleeding. For patients undergoing percutaneous coronary interventions, the addition of a short-term infusion of a glycoprotein IIb/IIIa receptor antagonist to aspirin prevents additional vascular events during the early in-hospital period but also increases the risk of major bleeding. Ongoing research is investigating other combinations of different antiplatelet drugs. In all these high-risk patients, there is a small excess of major bleeding among those assigned at random to aspirin, which is far outweighed by the magnitude of benefits on CVD. During an acute MI, after a loading dose of 160 mg to 325 mg aspirin, daily doses ranging from 75 to 150 mg daily are as effective as higher doses. For long-term treatment, the effects of doses < 75 mg daily are less certain. Although side effects are dose-related, especially in doses > 325 mg daily, no antiplatelet regimen is more effective than aspirin for long-term use. In primary prevention, 5 randomized trials have been published involving more than 60 000 apparently healthy men and women. Persons randomized to receive aspirin in these trials had significant reductions in risk of a first MI (32%) and important vascular events (15%). Since the numbers of strokes and vascular deaths were insufficient to distinguish between the benefits found in secondary prevention and no effect, use of aspirin in primary prevention should be weighed in light of the cardiovascular risk profile, the side effects of the drug, and its clear benefit in reducing risk of a first MI. Aspirin should be an adjunct, not an alternative, to managing other cardiovascular risk factors. Recently, the US Preventive Services Task Force and the American Heart Association recommended aspirin use for all men and women whose 10-year risks are > 6% and > or = 10%, respectively. In all these patient categories, including secondary prevention, acute MI and acute occlusive stroke, as well as primary prevention, increased and appropriate use of aspirin will prevent large numbers of premature deaths and MIs.

Aspirin↗
PubMed2005

[Comparative study of the results of coronary artery bypass grafting and angioplasty for myocardial revascularization in patients with equivalent multivessel disease].

OBJECTIVE: To investigate the relative efficacy of different therapeutic strategies in patients with symptomatic multivessel coronary artery disease with preserved ventricular function. The primary objectives were defined as a combination of death of cardiac origin, acute myocardial infarction (AMI), and refractory angina that required revascularization, and the secondary objectives were defined as anginal state and exercise-induced ischemia. METHODS: Of the 20,769 patients assessed on cine coronary angiography at InCor, 210 were chosen for this study and were randomized either for coronary artery bypass grafting (CABG, n = 105) or transluminal coronary angioplasty (TCA, n = 105). RESULTS: A mean of 3.2 +/- 0.8 vessels received anastomoses and 2.1 +/- 0.8 were successfully dilated in the CABG and TCA groups, respectively. In a 5-year follow-up, the rates of events in the CABG and TCA groups were, respectively: mortality, 9.52% and 12.38%; acute myocardial infarction, 2.85% and 8.57% (P = 0.0668); and additional intervention, 2.85% and 24.76% (P < 0.001). The survival rate was 88.39% for CABG and 84.93% for TCA; the respective AMI-free percentages were 84.40% and 77.40%. In the CABG and TCA groups, 62% and 60% of the patients had no angina, respectively. The exercise tests were considered nonischemic in 62.5% and 62.1% of the patients in the CABG and TCA groups, respectively. CONCLUSION: In multivessel patients, compared with angioplasty, coronary artery bypass grafting was associated with a lower incidence of long-term events and a reduced need for new interventions (P = 0.001).

Adult↗
PubMed2003

Reversible myocardial dysfunction, a possible complication in critically ill patients without heart disease.

PURPOSE: Reversible myocardial dysfunction or myocardial stunning is frequently described in patients with episodes of acute coronary syndrome and has recently been reported in critically ill patients without ischaemic heart disease. This article presents a study and description of the possible existence of myocardial dysfunction in critically ill patients in our setting who present no acute episode or history of cardiovascular disease. DESIGN: Prospective, descriptive study. SETTING: The intensive care unit of a district hospital. PATIENTS AND PARTICIPANTS: The study included all patients admitted to the intensive care unit between March 1998 and March 2001 for noncardiac causes and with no history of heart disease, and who underwent echocardiographic examination for electrocardiographic changes, signs of cardiac insufficiency, persistent arrhythmias, or any other indication. Patients with sepsis or other critical illness known to be associated with myocardial dysfunction were excluded from the study. The study was carried out on those selected patients who developed myocardial dysfunction. MEASUREMENTS AND RESULTS: Transthoracic and transoesophageal echocardiography were carried out to assess the left ventricular ejection fraction and any segmental contractility disturbances. These investigations were carried out within 24 hours of admission, during the first week, during the second or third week, after one month and after three to 6 months. The electrocardiogram was assessed on admission and the changes over time were studied. Thirty-three patients were included in the study after detecting myocardial dysfunction; the median age of these patients was 63 years [range, 23-82 years]. Seven patients died. The median initial left ventricular ejection fraction was 0.34 [range, 0.16-0.48] and improved with time. Segmental contractility disturbances were detected initially in all patients and also normalized with time. All patients presented electrocardiogram changes that normalised in line with the echocardiographic changes. CONCLUSIONS: Reversible myocardial dysfunction can be develop in critically ill patients without primary heart disease. This syndrome is associated with systolic dysfunction, segmental contractility disturbances and electrocardiographic changes.

APACHE↗
PubMed1999

Effects of nifedipine on myocardial blood flow and systolic function in humans with ischemic heart disease.

OBJECTIVE: To test the hypothesis that, in humans with ischemic heart disease, nifedipine is a primary dilator of the coronary circulation and in general exerts a net positive effect on the balance of myocardial oxygen supply and demand. METHODS: Positron-emission tomography with [13N]-ammonia was used to measure myocardial blood flow in patients at rest, and during infusion of adenosine and ingestion of nifedipine (10 mg capsule, a bite-and-chew technique). Myocardial segments were defined physiologically on the basis of blood flow to adenosine as being normal or having mild, moderate, or severe impairment of dilator reserve. Myocardial systolic function was assessed under comparable physiologic conditions using gated single-photon-emission computed tomography radionuclide ventriculography. RESULTS: Our study population consisted of 13 male patients and one female patient. Ingestion of nifedipine increased heart rate (from 63 +/- 11 to 80 +/- 16 beats/min, P < 0.001) and, as intended, lowered systolic arterial pressure (from 148 +/- 20 to 123 +/- 14 mmHg, P < 0.001) but had no effect on heart rate-pressure product (which changed from 9283 +/- 1576 to 9942 +/- 2162 mmHg/min). Myocardial blood flow in patients at rest in segments with mild, moderate, and severe reductions of dilator capacity (0.63 +/- 0.20, 0.67 +/- 0.25, and 0.58 +/- 0.27 ml/min per g, respectively) was less (P < 0.01) than normal (0.91 +/- 0.29 ml/min per g). Nevertheless, flow of blood was increased versus that at rest (P < 0.01) by infusion of adenosine (to 1.78 +/- 0.13, 1.29 +/- 0.16, and 0.75 +/- 0.22 ml/min per g) and ingestion of nifedipine (to 1.17 +/- 0.51, 1.06 +/- 0.36, 0.85 +/- 0.42 ml/min per g) in segments with mild, moderate, and severe reduction of dilator capacity as well as in normal segments (to 3.18 +/- 0.85 ml/min per g with adenosine and 1.68 +/- 0.65 ml/min per g with nifedipine). Global left ventricular systolic function remained unchanged versus baseline (ejection fraction 0.74 +/- 0.09) with nifedipine (0.76 +/- 0.10). Regional contraction expressed in normalized amplitude units also remained unchanged versus baseline in response to nifedipine. CONCLUSION: Nifedipine increases myocardial blood flow in humans with ischemic heart disease in normal segments as well as in segments with mild, moderate, and severe reductions of dilator capacity, albeit to a lesser extent with increasing impairment of dilator capacity. Both global and regional left ventricular contractile function also are not adversely affected by nifedipine. These improvements in myocardial blood flow in face of no change or a decrease in myocardial demand for oxygen reflect an overall favorable effect on the balance between the supply of and demand for myocardial oxygen.

Aged↗
PubMed1999

Evidence of exercise-induced myocardial ischemia in patients with primary aldosteronism: the Cross-sectional Primary Aldosteronism and Heart Italian Multicenter Study.

BACKGROUND: Primary aldosteronism (PA) is a disease associated with hypersecretion of aldosterone caused by an aldosterone-producing adrenal adenoma, bilateral adrenal hyperplasia, and, although rarely, by adrenal carcinoma. Arterial hypertension induces several cardiovascular alterations that yield a high cardiovascular risk. It has been shown that reduced myocardial perfusion at rest, assessed by thallium-201 myocardial scintigraphy, was greater in PA than in essential hypertension (EH). However, it is still unknown whether reduced myocardial perfusion at rest and/or regional function abnormalities are present during exercise-induced myocardial stress. PURPOSE: We addressed the impact of PA on myocardial ischemia and sought to identify signs of exercise-induced myocardial ischemia (assessed by MIBI-SPECT and echocardiography) in patients with PA compared to patients with EH. Patients with consistent signs of myocardial ischemia on all of the tests were studied by coronary arteriography. PATIENTS: We studied 72 patients with PA and an age/sex-matched group of 72 patients with EH enrolled in the cross-sectional Primary Aldosteronism and Heart Italian Multicenter Study (PAHIMS). METHODS: Regional function was detected from echocardiographic measurement of wall motion done at baseline and immediately after exercise. Myocardial perfusion was evaluated by SPECT imaging after injecting 99mTc-MIBI with the same-day protocol using the rest-stress sequence. RESULTS: Although the conditions of arterial pressure, duration of hypertension, and target organ damage were equivalent, the patients with PA had greater incidence of both reversible perfusion defects and abnormalities of regional function. Moreover, multiple regression analysis showed that the high plasma aldosterone level was highly predictive for SPECT ischemic score and wall motion index, suggesting that PA contributes to cardiovascular risk over and above that associated with ventricular hypertrophy. Exercise-induced myocardial ischemia in PA was not segmental but widely distributed suggesting that this phenomenon was not related to abnormal coronary perfusion. Accordingly, of the 38 patients with PA who underwent coronarography, there was no presence of significant coronary atherosclerotic lesions in 30 (78.9%) of the patients. CONCLUSIONS: The PAHIMS observed more exercise-induced moderate myocardial ischemic defects (co-detected by SPECT and echocardiograms and not segmental but widely allocated) in patients with PA than in patients with EH. This phenomenon occurred in a greater percentage of patients with PA without significant coronary lesions (78.95%, n = 38), which supports the possible presence of small-vessel intramyocardial disease.

Adult↗
PubMed2000

Secondary prevention with antioxidants of cardiovascular disease in endstage renal disease (SPACE): randomised placebo-controlled trial.

BACKGROUND: Excess cardiovascular mortality has been documented in chronic haemodialysis patients. Oxidative stress is greater in haemodialysis patients with prevalent cardiovascular disease than in those without, suggesting a role for oxidative stress in excess cardiovascular disease in haemodialysis. We investigated the effect of high-dose vitamin E supplementation on cardiovascular disease outcomes in haemodialysis patients with pre-existing cardiovascular disease. METHODS: Haemodialysis patients with pre-existing cardiovascular disease (n=196) aged 40-75 years at baseline from six dialysis centres were enrolled and randomised to receive 800 IU/day vitamin E or matching placebo. Patients were followed for a median 519 days. The primary endpoint was a composite variable consisting of: myocardial infarction (fatal and non-fatal), ischaemic stroke, peripheral vascular disease (excluding the arteriovenous fistula), and unstable angina. Secondary outcomes included each of the component outcomes, total mortality, and cardiovascular-disease mortality. FINDINGS: A total of 15 (16%) of the 97 patients assigned to vitamin E and 33 (33%) of the 99 patients assigned to placebo had a primary endpoint (relative risk 0.46 [95% CI 0.27-0.78], p=0.014). Five (5.1%) patients assigned to vitamin E and 17 (17.2%) patients assigned to placebo had myocardial infarction (0.3 [0.11-0.78], p=0.016). No significant differences in other secondary endpoints, cardiovascular disease, or total mortality were detected. INTERPRETATION: In haemodialysis patients with prevalent cardiovascular disease, supplementation with 800 IU/day vitamin E reduces composite cardiovascular disease endpoints and myocardial infarction.

Aged↗
PubMed2001

Prevalence and risk factors of clinical diabetic polyneuropathy in a Portuguese primary health care population.

OBJECTIVE: Distal symmetrical polyneuropathy in diabetics (DPN) has a variable prevalence around 30% and increases the risk for foot ulcers and amputations. We aimed at evaluating the prevalence of clinical DPN and associated risk factors in patients followed in primary care centers. MATERIAL AND METHODS: 101 type 2 diabetics were evaluated and 8 were excluded due to the presence of other causes of neuropathy. The remaining 93 had a mean age of 65.4 +/- 10.1 years and a mean diabetes duration of 10.1 +/- 11.1 years, 60.2% were women and 39.8% men. DPN was defined as the presence of both altered sensitivities and reflexes, regardless of symptoms. RESULTS: Seventy-two (80%) patients had symptoms of polyneuropathy, but DPN was present only in 29 (32.2%). Calluses (37.8%) and trophic skin (74.4%) and nail (75.6%) changes were found in both feet. There was a significant positive association of DPN with age (69.0 +/- 9.1 vs 63.3 +/- 9.9 years, p=0.01), disease duration (15.7 +/- 13.5 vs 7.2 +/- 8.8 years, p=0.001), feet skin changes (38.8 vs 13.0%, p=0.04) and myocardial infarction/ischemia (14.8 vs 1.7%, p=0.03). CONCLUSIONS: This sample of diabetic patients cared by family doctors presented a high prevalence of DPN. Aging, disease duration, the presence of feet skin changes and myocardial infarction/ischemia are factors that increase the prevalence of the disease. Primary care doctors awareness of the problem might help to decrease the associated morbidity.

Aged↗
PubMed2004

Use of losartan in diabetic patients in the primary care setting: review of the results in LIFE and RENAAL.

OBJECTIVE: To review outcomes of diabetic patients treated with losartan in two recent randomized, double-blind, clinical trials and compare outcomes to similar studies in diabetics. METHODS: The Reduction in ENdpoints with the Angiotensin II Antagonist Losartan (RENAAL) study recruited 1513 patients with type 2 diabetes and nephropathy. The Losartan Intervention For Endpoint reduction (LIFE) study recruited 9193 hypertensive patients with left ventricular hypertrophy (LVH) including 1195 with diabetes mellitus. The maximum losartan dose in both studies was 100 mg daily. All study patients could receive additional antihypertensive medications, excluding angiotensin converting enzyme inhibitors (ACEIs) and other angiotensin receptor blockers (ARBs), if blood pressures (BP) < 140/90 mmHg were not achieved. In RENAAL, the control group received placebo whereas in LIFE, controls received atenolol. BP reductions were comparable in the treatment and control groups of both studies. In RENAAL, the primary outcome was the composite of doubling of serum creatinine, end-stage renal disease, or death. In LIFE, the primary composite outcome was cardiovascular death and non-fatal myocardial infarction or stroke. RESULTS: In RENAAL, losartan reduced the primary composite end-point 16% (p = 0.02) and the incidence of end-stage renal disease (ESRD) 28% (p = 0.002). In LIFE, the primary composite endpoint among diabetics was reduced 24% (p = 0.03), cardiovascular mortality was reduced 37% (p = 0.03) and total mortality was reduced 39% (p = 0.002). DISCUSSION: In diabetic patients with nephropathy, losartan reduces progression to endstage renal disease. In hypertensive diabetic patients with LVH, losartan reduces cardiovascular morbidity and mortality and total mortality. Angiotensin receptor blockade with losartan appears to confer benefits beyond BP reduction in diabetic patients at high-risk for cardiovascular and renal events.

Aged↗
PubMed1984

Emergency evaluation of the cancer patient.

The oncology patient can experience medical or surgical emergencies as a result of effects of the primary tumor, metastases, or systemic effects of the disease. Emergencies unrelated to the primary oncologic diagnosis, such as acute myocardial infarction, drug overdose, or gastrointestinal hemorrhage, also may occur. For this reason routine emergency protocols and diagnostic procedures should be followed in the treatment of oncology patients. We review the major oncologic-related emergencies, including central nervous system and spinal cord compression, airway obstruction, cardiac tamponade, gastrointestinal obstruction, adrenal insufficiency and hypercalcemia, sepsis, and coagulopathies. Medical and surgical emergencies in the oncology patient should be treated aggressively in the emergency department because a determination about the quality of life of the patient, or the reversibility of the acute process, often cannot be answered quickly in the emergency setting.

Airway Obstruction↗
PubMed1992

Predicting the prevalence of a disease in a cohort at risk.

A non-homogeneous Markov chain model is used to describe the evolution of a progressive chronic disease. Transition probabilities are estimated from data on coronary heart disease in Australia. By varying the transition probabilities, the effects of changes in medical management or in the natural history of the disease are examined. For reducing rates of fatal and non-fatal acute myocardial infarction a multifaceted strategy of primary and secondary prevention and improved acute care is found most effective. Primary prevention reducing the risk of early stages of the disease has the potential to yield the highest proportion of disease-free people. By contrast, intensive medical treatment of acute disease would reduce mortality but increase the total burden of disease in the population.

Adult↗
PubMed2007

Impact of diabetes on five-year outcomes of patients with multivessel coronary artery disease.

BACKGROUND: Diabetes mellitus is a major cause of coronary artery disease. Despite improvement in the management of patients with stable coronary artery disease, diabetes remains a major cause of increased morbidity and mortality. Although coronary artery bypass grafting surgery (CABG) and percutaneous coronary intervention are widely used, no conclusive evidence exists that either treatment modality is better than medical therapy alone for the treatment of stable single- or multivessel coronary disease in patients with diabetes. METHODS: We compared medical therapy, percutaneous coronary intervention, and CABG in 499 diabetic patients (38.5%) and 799 nondiabetic patients (61.5%) with single- or multivessel coronary disease. The composite primary endpoint was cardiac-related death, Q-wave myocardial infarction, or refractory angina requiring revascularization. RESULTS: We treated 1,298 patients with either CABG (n = 524), percutaneous coronary intervention (n = 378), or medical therapy (n = 396). More deaths occurred among patients with diabetes than among patients without diabetes, regardless of which option was used (p < 0.001). When treatment modalities were stratified according to the number of diseased vessels, CABG was shown to be more beneficial for patients with diabetes and multivessel disease than for patients with diabetes and single-vessel disease (p < 0.001). However, when stratified by treatment, patients with diabetes receiving medical therapy had a worse prognosis than patients with diabetes treated with CABG (p = 0.005). CONCLUSIONS: All three therapeutic regimens resulted in high rates of cardiac-related deaths among patients with diabetes compared with patients without diabetes. Moreover, we observed better outcomes among patients with diabetes and multivessel coronary artery disease undergoing CABG regarding the primary endpoint at 5-year follow-up.

Adult↗
PubMed1993

Primary and secondary prevention of myocardial infarction and strokes: an update of randomly allocated, controlled trials.

AIM: To summarize the risk factors associated with coronary heart disease and strokes and to evaluate measures used in the prevention and treatment of these diseases. METHOD: A review of the results of randomly allocated clinical trials of treatment for both primary and secondary prevention of coronary heart disease and strokes. RESULTS: Reductions in elevated blood pressure and cholesterol and cessation of cigarette smoking have clearly been shown to reduce the incidence of coronary heart disease. A reduction in blood pressure has also been shown to reduce the risk of strokes. In addition to other classical risk factors, such as abnormal serum lipids, diabetes and a genetic predisposition, recent studies have shown that elevated levels of fibrinogen and other clotting factors, elevated levels of renin and decreased levels of anti-oxidant vitamins such as E, C and beta-carotene can predict coronary heart disease and strokes. Thrombolytic therapy, aspirin and beta-blockers have been shown to reduce mortality in patients with myocardial infarction, and the latter two agents reduce mortality, re-infarction and strokes with long-term use. Treatment with intravenous magnesium and nitrates has shown promise but larger trials are required to confirm the results. Both aspirin and heparin have proven value in reducing the incidence of myocardial infarction and death in unstable angina. Following an acute myocardial infarction, long-term therapy with aspirin, beta-blockers, lipid-lowering agents and oral anticoagulants has been shown to reduce mortality and re-infarction. In patients with large infarcts associated with a low ejection fraction or heart failure, the use of angiotensin converting enzyme (ACE) inhibitors reduces mortality, hospitalization for heart failure and re-infarction. The use of diuretics to lower blood pressure reduces strokes. In contrast, calcium antagonists do not appear to consistently reduce mortality or prevent vascular events when used for primary or secondary prevention of either myocardial infarction or strokes. CONCLUSIONS: Myocardial infarction and strokes can be prevented by refraining from smoking and maintaining appropriate blood pressure levels and a favourable balance of lipids. Following a myocardial infarction, further drug treatment should include aspirin, thrombolytic therapy (in acute myocardial infarction), beta-blockers, ACE inhibitors (in patients with a low ejection fraction) and perhaps anticoagulants.

Adrenergic beta-Antagonists↗