The objective of this prospective study was to examine the association between serum levels of TNF (tumor‐necrosis factor) and IL‐6 (interleukin‐6) and left ventricular mass in hypertensive patients. Hypertensive patients currently receiving medical therapy were eligible. All subjects underwent echocardiography with measurements of left ventricular (LV) mass and ejection fraction (EF) and had serum levels of TNF and IL‐6 measured by ELISA immunoassay. 35 subjects (20F, 15M; mean age 56.4±10.5yrs) were studied. 19 patients (54%) had elevated LV mass. Of these patients, 6 (32%) had detectable serum TNF levels and 6 (32%) detectable IL‐6 levels. Of the 16 patients with LV mass within normal limits, 2 (14%) had detectable TNF levels and 1 (7%) had detectable IL‐6 levels. (p = NS). Hypertensive patients with elevated LV mass do not consistently exhibit elevated cytokine levels when compared to those with normal LV mass.

Elevated levels of troponin T have been demonstrated in number of studies to be a strong, independent prognostic indicator in patients with acute coronary syndromes [ 1 Ohman M.E. et al. for the GUSTO-II a InvestigatorsCardiac troponin T levels for risk stratification in acute myocardial ischemia. N. Engl. J. Med. 1996; 335: 1333-1341 Crossref PubMed Scopus (1008) Google Scholar , 2 Ravkilde J. Nissen H. Horder M. et al. Independent prognostic value of serum creatine kinase isoenzyme MB mass, cardiac troponin T and myosin light chain levels in suspected acute myocardial infarction: analysis of 28 months follow-up in 196 patients. J. Am. Coll. Cardiol. 1995; 25: 574-581 Abstract Full Text PDF PubMed Scopus (231) Google Scholar , 3 Lindahl B. Venge P. Wallentin L. Relation between troponin T and the risk of subsequent cardiac events in unstable coronary artery disease. Circulation. 1996; 93: 1651-1657 Crossref PubMed Scopus (553) Google Scholar , 4 Stubbs P. Collinson P. Moseley D. et al. Prospective study of the role of cardiac troponin T in patients admitted with unstable angina. BMJ. 1996; 313: 262-264 Crossref PubMed Scopus (177) Google Scholar , 5 Luscher M.S. Thygesen K. Ravkilde J. et al. Applicability of cardiac troponin T and I for early risk stratification in unstable angina. Circulation. 1997; 96: 2578-2585 Crossref PubMed Scopus (237) Google Scholar , 6 Braunwald E. Antman E.M. et al. ACC/AHA guidelines. Circulation. 2000; 102: 1193-1209 Crossref PubMed Scopus (566) Google Scholar , 7 La Vecchia L. Mezzena G. Ometto R. et al. Detectable serum troponin I in patients with heart failure of non-myocardial ischemic origin. Am. J. Cardiol. 1997; 80: 88-90 Abstract Full Text PDF PubMed Scopus (113) Google Scholar ]. In acute and chronic heart failure increased serum levels of troponin I and troponin T were also found to correlate with a poorer prognosis [ 8 Sato Y. Yamada T. Taniguchi R. et al. Persistently increased serum concentrations of cardiac troponin T in patients with idiopathic dilated cardiomyopathy are predictive of adverse outcome. Circulation. 2001; 103: 369-374 Crossref PubMed Scopus (271) Google Scholar , 9 La Vecchia L. Mezzena G. Zanolla L. et al. Cardiac troponin I as diagnostic and prognostic marker in severe heart failure. J. Heart Lung Transplant. 2000; 19: 644-652 Abstract Full Text Full Text PDF PubMed Scopus (173) Google Scholar , 10 Logeart D. Beyne P. Cusson C. et al. Evidence of cardiac myolysis in severe non ischemic heart failure and the potential role of increased wall strain. Am. Heart J. 2001; 141: 247-253 Abstract Full Text Full Text PDF PubMed Scopus (121) Google Scholar , 11 Missov E. Calzolari C. Pau B. Circulating cardiac troponin T in severe congestive heart failure. Circulation. 1997; 96: 2953-2958 Crossref PubMed Scopus (362) Google Scholar , 12 Missov E. Mair J. A novel biochemical approach to congestive heart failure: cardiac troponin T. Am. Heart J. 1999; 138: 95-99 Abstract Full Text Full Text PDF PubMed Scopus (139) Google Scholar ]. A recent report has documented an overall poor prognosis in patients with acute pulmonary edema and elevated troponin T levels [ [13] Ishii J. Nomura M. Nakamura Y. et al. Risk stratification using a combination of cardiac troponin T and brain natriuretic peptide in patients hospitalized for worsening chronic heart failure. Am. J. Cardiol. 2002; 89: 691-695 Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar ]. While pulmonary edema may often be secondary to acute ischemia, other causes such as hypertensive crisis and volume overload may precipitate decompensated heart failure and pulmonary edema [ [1] Ohman M.E. et al. for the GUSTO-II a InvestigatorsCardiac troponin T levels for risk stratification in acute myocardial ischemia. N. Engl. J. Med. 1996; 335: 1333-1341 Crossref PubMed Scopus (1008) Google Scholar ]. Distinguishing ischemia-induced pulmonary edema from pulmonary edema due to other causes is a difficult clinical challenge with important implications for clinical management [ 14 Goldberger J.J. Peled H.B. Stroh J.A. et al. Prognostic factors in acute pulmonary edema. Arch. Intern. Med. 1986; 146: 489-493 Crossref PubMed Scopus (68) Google Scholar , 15 Wiener R.S. Moses H.W. Richeson J.F. et al. Hospital and long-term survival of patients with acute pulmonary edema associated with coronary artery disease. Am. J. Cardiol. 1987; 60: 33-35 Abstract Full Text PDF PubMed Scopus (25) Google Scholar , 16 Roguin A. Behar D. Ben Ami H. et al. Long-term prognosis of acute pulmonary edema—an ominous outcome. Eur. J. Heart Fail. 2000; 2: 137-144 Crossref PubMed Scopus (62) Google Scholar , 17 Plotnick G.D. Kelemen M.H. Garrett R.B. et al. Acute cardiogenic pulmonary edema in the elderly: factors predicting in-hospital and one-year mortality. South Med. J. 1982; 75: 565-569 Crossref PubMed Scopus (38) Google Scholar ].

Left ventricular hypertrophy (LVH) is an independent predictor of cardiovascular risk, particularly in hypertensive patients. These patients are frequently referred for echocardiographic assessment of LVH to help guide medical therapy. In clinical practice generally, LVH is assessed by measurement of wall thickness alone and not by validated calculations of LV mass. In addition, LV mass is not indexed by body surface area or by gender as is recommended. The objective of this prospective study was to compare assessment of LVH by echo using measurement of wall thickness alone (WT) to that using calculation of LV mass (LVM) and indexed to body surface area and gender. Patients with a clinical history of hypertension who were referred for echocardiography were entered into the study. All underwent standard 2-D and m-mode echocardiography with measurement of LV wall thickness. LV mass was calculated according to a necropsy validated formula of LV mass (grams) = 0.8 X (1.04 X ((septal thickness + LV internal diameter + posterior wall thickness)3 – (LV internal diameter)3)) + 0.6 and indexed to body surface area. For each patient, the presence of LVH was assessed by both methods with LVH defined as wall thickness ≥ 12mm by WT and as mass >131g/m2 in men and 100g/m2 in women by LVM. 92 patients (50M/42F) were entered into the study. In only 61 patients (66%), were the two methods concordant with 24 patients having LVH by both methods and 37 without LVH by both methods. In 31 patients (34%), assessment of LVH was discordant with 19 patients having LVH by WT in the presence of normal LV mass by LVM and 12 patients without LVH by WT having documented LVH by LVM. When assessed by gender, there was a tendency for WT to underestimate LVH in females (sensitivity 45%, specificity 85%) and overestimate LVH in males (sensitivity 100%, specificity 56%). Measurement of wall thickness overestimates LVH in males and underestimates LVH in females and should not be used as a surrogate marker for increased LV mass. Echocardiographic assessment of LVH and clinical decision-making in hypertensive patients should be based on calculation of LV mass indexed for body surface area and gender. Am J Hypertens (2004) 17, 84A–85A; doi: 10.1016/j.amjhyper.2004.03.216

Background An increasing number of patients have an acute coronary syndrome while abroad. Such an event may entail significant emotional and financial stress, and patients are usually anxious to return home as soon as possible. The safety of long-distance air travel soon after an acute coronary syndrome is, however, uncertain, and few data exist regarding the evaluation of such patients, the proper timing and conditions of the flight,and short-term complications.Methods and Results We prospectively evaluated 21 tourists who had an acute coronary syndrome in Jerusalem. Patients at high risk were offered angiography; others underwent stress testing. Telephone interviews were conducted a few weeks after the patients returned home, and follow-up information was obtained. Patients flew home 18.2 +/- 11 days (mean +/- SD) after the acute event. Flight duration was substantial (12.5 +/- 3 hours). No patient had cardiac symptoms en route. At follow-up (21.3 +/- 13 days), all but 2 patients were alive and free of cardiac symptoms.Conclusions A long-distance flight within 2 to 3 weeks after an acute coronary syndrome is reasonably safe, provided significant ischemia is excluded or treated.

Background In patients with acute myocardial infarction (MI), early fibrinolytic therapy results in improved survival and preservation of ventricular function. The purpose of the study was to determine whether very early treatment also reduces the development of congestive heart failure. Methods and Results During the years 1984 to 1989, 358 consecutive patients with acute MI were treated with streptokinase, 161 within the first 1.5 hours from the onset of chest pain (group A) and 197 within 1.5 to 4.0 hours (group B). In 68, fibrinolysis was initiated in the prehospital setting pioneered by our group. Symptoms related to heart failure including dyspnea on exertion, fatigue, orthopnea, paroxysmal nocturnal dyspnea, nocturia, and peripheral edema, in addition to pulmonary edema events, were assessed during 5 years of follow-up. The evaluation was based on medical records and a detailed questionnaire, which was filled in by the investigators. A favorable significant effect of very early thrombolysis on the development of most of these limiting symptoms appeared 3 months after hospital discharge and persisted thereafter (P <.05). During hospitalization, pulmonary edema attacks occurred less frequently in patients from group A (23% vs 36.5%, P <.01). This difference persisted during 4 years of follow-up (13% vs 36%, P <.001). Conclusions Our data demonstrate that very early fibrinolytic therapy results in a significant long-term reduction of congestive heart failure–related symptoms and thereby improves the quality of life in patients after MI. (Am Heart J 2000;139:1096-100.)

Objectives The study sought to determine the 6-month clinical outcome of patients who underwent implantation of very long coronary stents to treat diffuse disease and/or long dissections and to compare the findings with those reported in the literature for patients who underwent implantation of multiple short coronary stents.Background New designs of flexible stents enable the implantation of long stents rather:han multiple short, older design stents. The initial experience is very promising but the long-term outcome has not been described yet.Methods Fifty-seven consecutive patients in whom 67 long stents (greater than or equal to 30 mm) were successfully deployed were included in this study. Six-month clinical and angiographic follow-up was prospectively collected, patients with recurrent angina underwent coronary angiography without further testing. patients who remained asymptomatic at the 6-month follow-up visit underwent positron emission tomographic imaging, and those with results suggestive of ischemia underwent coronary angiography. A combined study end point was defined as death, myocardial infarction, and the need for target vessel revascularization.Results Only 1 patient (2%) reached a study end point at hospital discharge. An additional 20 patients (total 21 patients [37%]) reached an end point by 6 months. The outcome was not influenced by the clinical presentation (stable or unstable angina) or by the indication for stenting (elective or emergency). Predictors For adverse outcome were multiple stents per narrowing (63% vs 29%, P <.04), and stents smaller than 3.5 mm (49% vs 22%). Narrowing and stent length were not predictive of a study end point in narrowings that were successfully treated by a single long stent.Conclusions Elective stenting provides an effective solution for patients with diffuse coronary disease provided that ct single long stent (usually <40 mm) can cover the full length of the narrowing. The results are better when vessels larger than 3 mm are treated. Compared with multiple short stents, implantation of a single long stent is probably at least as effective, and the procedure is quicker and cheaper and thus should be the preferred approach.

This paper will review the hypothesis that early complete thrombolytic therapy in acute myocardial infarction reduces mortality and improves prognosis. ACE inhibitors improve remodelling and anti-platelet drugs or interventional procedures prevent reocclusion of the infarct related coronary artery. Most patients are left with significant myocardial damage and this effect is cumulative with subsequent infarction. The average age of death has increased by 10 years in the last three decades, so that many older patients survive. They have survived acute myocardial infarction and we now have a significant population with important heart failure despite good thrombolytic therapy.

The long term impact of pre-hospital thrombolysis in acute myocardial infarction on the subsequent development of heart failure symptoms was investigated in 362 consecutive patients. The pre hospital strategy, used in 61 patients, allowed for very early administration of streptokinase, within 1.2+/-0.6 (mean+/-S.D.) hours from pain onset. In contrast, 294 patients treated in hospital received lytic treatment within 2.0+/-0.9 hours. The pre hospital group showed faster reperfusion, as measured by the time to peak creatine kinase and to ST segment recovery, but only a slightly better ventricular function, as compared to hospital treated patients. Heart failure symptoms were significantly reduced in the pre hospital group during hospitalization and at long term follow up: there were less dyspnea, fatigue, orthopnea, nocturnal dyspnea, nocturia, peripheral edema and episodes of pulmonary edema. Angina was reduced as well. We conclude that the initial benefit of prehospital thrombolysis translates into long term reduction of heart failure symptoms, thus improving quality of life.

Apoplexy of a previously asymptomatic pituitary macroadenoma may occur in the setting of intensive thrombolytic, antithrombotic, or anticoagulant therapy for acute myocardial infarction. Classic clinical findings may initially be nonspecific and a high index of suspicion is therefore required for early diagnosis.

Bloody tamponade is an unusual complication of post-infarction pericarditis. The major cause of hemopericardium in this setting is left ventricular free wall rupture. We report a case of post-infarction hemorrhagic pericarditis mimicking subacute rupture of the left ventricular free wall.

Acute myocardial infarction occurs when a ruptured coronary artery plaque causes sudden thrombotic occlusion of a coronary artery and cessation of coronary artery blood flow. This paper reviews the underlying coronary pathology in progressive coronary atherosclerosis, mechanisms of plaque rupture and arterial occlusion and the time relationship between coronary occlusion and myocardial necrosis. Reperfusion can be achieved by chemical thrombolysis with different thrombolytic agents. Early lysis is achieved best by prehospital administration, a transtelephonic monitor, a mobile intensive care unit, active general practitioner treatment or by warning the emergency room of impending arrival of a patient. Thrombolytic therapy may be unsuccessful and not achieve Grade III TIMI flow in less than 4 h (or even 2 h) due to inadequate or intermittent perfusion or reocclusion. Adjuvant therapy includes aspirin and platelet receptor antagonists. Bleeding is a constant danger. Direct percutaneous transluminal coronary angioplasty (PTCA) may be as effective or better than chemical thrombolysis. Reperfusion protects the myocardium and salvages viable tissue. It also improves mechanical remodelling of the ventricle. Long-term follow-up has shown that quantum leaps of fresh coronary occlusion causes step-wise progression in patient disability and that further early, prompt reperfusion can salvage myocardium and prevent this inexorable progress of the disease.

The presence of an intracranial space-occupying lesion (SOL) is considered an absolute contraindication to thrombolytic therapy during acute myocardial infarction (AMI)1Habib G.B. Current status of thrombolysis in acute myocardial infarction: II. Optimal utilization of thrombolysis in clinical subsets.Chest. 1995; 107: 528-534Abstract Full Text Full Text PDF PubMed Scopus (7) Google Scholar because such lesions are potential sites for intracranial hemorrhage. Patients with an SOL were therefore excluded from thrombolytic trials. We report a case of inadvertent thrombolysis in a patient with an intracranial meningioma. A 62-year-old woman was admitted to our hospital complaining of left-sided chest pain of 1-h duration. The patient claimed to be healthy. On hospital admission, the BP was 120/80 mm Hg and the pulse rate was 100 beats/min and regular. Results of the physical examination were otherwise normal. An ECG revealed normal sinus rhythm with 5-mm ST segment elevation in leads V1 through V6. The patient received 1.5 million units of IV streptokinase, as well as aspirin, propranolol, IV heparin, and nitroglycerin. The chest pain resolved within minutes of streptokinase administration and the ECG evolution was compatible with successful reperfusion. The following day, the patient disclosed that 4 years previously, after having developed vertigo, an MRI of the brain had demonstrated a dura-based left cerebellopontine angle lesion 1 cm in diameter consistent with a meningioma. During follow-up, no neurologic defects had appeared and the lesion had not enlarged. Despite the presence of an SOL, anticoagulant therapy was continued without neurologic sequela and the patient was discharged from the hospital in good health. Thrombolytic therapy reduces early mortality in patients with extensive acute anterior wall myocardial infarction by 25 to 50%.2Fibrinolytic Therapy Trialists' (FTT) Collaborative GroupIndications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomized trials of more than 1,000 patients.Lancet. 1994; 343: 311-322Abstract PubMed Scopus (2854) Google Scholar Among patients recruited to the major thrombolytic trials, the overall risk of intracranial hemorrhage was 0.75%, but ranged from 0.26 to 2.17%.3Simoons M.L. Maggioni A.P. Knatterud G. et al.Individual risk assessment for intracranial haemorrhage during thrombolytic therapy.Lancet. 1993; 342: 1523-1528Abstract PubMed Scopus (271) Google Scholar Risk factors for bleeding include age, body weight less than 70 kg, hypertension on hospital admission, and alteplase therapy.3Simoons M.L. Maggioni A.P. Knatterud G. et al.Individual risk assessment for intracranial haemorrhage during thrombolytic therapy.Lancet. 1993; 342: 1523-1528Abstract PubMed Scopus (271) Google Scholar Intracranial meningiomas are common, but rarely cause hemorrhagic stroke4Kohli C.M. Crouch R.L. Meningioma with intracerebral hematoma.Neurosurgery. 1984; 15: 237-240Crossref PubMed Scopus (53) Google Scholar and are not considered an absolute contraindication to anticoagulation. A computerized MEDLINE search from 1966 to 1996 revealed no reports of thrombolytic therapy in patients with an intracranial meningioma. Because of logistic considerations, timely direct coronary angioplasty is not a realistic alternative to thrombolytic therapy for most patients presenting with AMI.5Lange R.A. Hillis L.D. Immediate angioplasty for acute myocardial infarction [editorial].N Engl J Med. 1993; 328: 726-728Crossref PubMed Scopus (42) Google Scholar A physician must decide for each individual patient whether the potential benefits of thrombolytic therapy outweigh the risks. We suggest that if a patient with an intracranial meningioma presents with an extensive anterior wall AMI, and direct coronary angioplasty is not available, thrombolytic therapy may be considered and could prove lifesaving.

Objectives. We sought to compare the angiographic outcome of diabetic patients (treated with insulin or oral hypoglycemic agents) after successful coronary angioplasty with that in nondiabetic patients. The analysis included the outcome of the dilated (restenosis) and nondilated narrowings (disease progression).Background. Recent data have confirmed that diabetes mellitus is an important risk factor for long term adverse events. These adverse events are more common after balloon angioplasty than after bypass surgery (Bypass Angioplasty Revascularization Investigation [BARI]).Methods. We examined retrospectively 353 coronary angiograms of 248 patients (55 diabetic, 193 nondiabetic),who were referred for diagnostic angiography >1 month after successful angioplasty (1.4 +/- 0.6 [mean +/- SD] repeat angiograms/patient). Restenosis and disease progression/regression were compared between groups by means of quantitative angiography.Results. Baseline clinical and angiographic characteristics were similar in both groups, There was a nonsignificant trend for a higher restenosis rate of dilated narrowings in diabetic patients. There were no significant changes between diabetic and nondiabetic patients in the rates df progression and regression of narrowings that were not dilated during the initial angioplasty. The main difference was in the rate of appearance of new narrowings: There was a 22% increase in the number of narrowings on the follow-up angiogram in diabetic patients (38 new, 174 preexisting narrowings) compared with 12% (86 new, 734 preexisting narrowings) in nondiabetic patients (p < 0.004). Diabetes mellitus and the performance of angioplasty in the artery had an additive risk for development of new narrowings, which were identified in 15 (16.9%) of 89 arteries with and 16 (13.2%) of 121 without angioplasty in diabetic patients and in 42 (12.7%) of 331 arteries with and 38 (7.3%) of 518 without angioplasty in nondiabetic patients (p = 0.009).Conclusions. The combination of diabetes mellitus and an artery that was instrumented during balloon angioplasty is additive and increases the risk of formation of new narrowing in that artery. This finding may explain the high adverse event rates observed in diabetic patients in the angioplasty arm of the BARI study, most of whom had angioplasty performed in at least two arteries. (C) 1997 by the American College of Cardiology.