Aaron Frimerman

Increased expression of the CD11b/CD18 antigen on the surface of peripheral white blood cells in patients with ischemic heart disease: further evidence for smoldering inflammation in patients with atherosclerosis.

BACKGROUND This study examined the availability of the CD11b/CD18 and CD62L antigens on the surface of peripheral blood leukocytes in patients with ischemic heart disease. METHODS AND RESULTS The study population included 45 patients with angiographically documented ischemic heart disease admitted to our department of internal medicine and the cardiology department during 1 month (December 1997). Sixty-six healthy members of the hospital medical staff served as control subjects. Another 39 post-trauma patients who were admitted to the emergency room were also evaluated. Patients with ischemic heart disease had significantly (P <.002) higher concentrations of CD11b/CD18 antigen on the surface of their polymorphonuclear leukocytes and monocytes (mean fluorescence intensity of 203 +/- 81 and 261 +/- 75, respectively) compared with the control group (mean fluorescence intensity 158 +/- 68 and 211 +/- 74, respectively) and to the group of patients with acute stress (mean fluorescence intensity of 146 +/- 70 and 200 +/- 22, respectively). CONCLUSIONS The presence of increased concentration of CD11b/CD18 suggests that circulating leukocytes are activated in patients with ischemic heart disease. This activation probably reflects the presence of an inflammatory response involving the atherosclerotic lesion and is not merely a result of acute stress.

Non-Invasive Lung IMPEDANCE-Guided Preemptive Treatment in Chronic Heart Failure Patients: A Randomized Controlled Trial (IMPEDANCE-HF Trial)

BACKGROUND Previous investigations have suggested that lung impedance (LI)-guided treatment reduces hospitalizations for acute heart failure (AHF). A single-blind 2-center trial was performed to evaluate this hypothesis (ClinicalTrials.gov-NCT01315223). METHODS The study population included 256 patients from 2 medical centers with chronic heart failure and left ventricular ejection fraction ≤35% in New York Heart Association class II-IV, who were admitted for AHF within 12 months before recruitment. Patients were randomized to a control group treated by clinical assessment and a monitored group whose therapy was also assisted by LI, and followed for at least 12 months. Noninvasive LI measurements were performed with a new high-sensitivity device. Patients, blinded to their assignment group, were scheduled for monthly visits in the outpatient clinics. The primary efficacy endpoint was AHF hospitalizations; the secondary endpoints were all-cause hospitalizations and mortality. RESULTS There were 67 vs 158 AHF hospitalizations during the first year (P < .001) and 211 vs 386 AHF hospitalizations (P < .001) during the entire follow-up among the monitored patients (48 ± 32 months) and control patients (39 ± 26 months, P = .01), respectively. During the follow-up, there were 42 and 59 deaths (hazard ratio 0.52, 95% confidence interval 0.35-0.78, P = .002) with 13 and 31 of them resulting from heart failure (hazard ratio 0.30, 95% confidence interval 0.15-0.58 P < .001) in the monitored and control groups, respectively. The incidence of noncardiovascular death was similar. CONCLUSION Our results seem to validate the concept that LI-guided preemptive treatment of chronic heart failure patients reduces hospitalizations for AHF as well as the incidence of heart failure, cardiovascular, and all-cause mortality.

Transient ST-elevation myocardial infarction: clinical course with intense medical therapy and early invasive approach, and comparison with persistent ST-elevation myocardial infarction.

Patients presenting with ST-elevation myocardial infarction (STEMI), whose symptoms and electrocardiographic changes completely resolve upon admission and before the administration of reperfusion therapy, pose a therapeutic dilemma. The optimal management of this syndrome, termed here as transient STEMI (TSTEMI), has not yet been fully determined. We describe 69 prospectively recorded patients with TSTEMI, of which 63 patients (56.7 +/- 11 years, 48 men) were available for long-term follow-up out of 1244 consecutive patients with acute myocardial infarction (5%). Patients with TSTEMI treated with intravenous isosorbide dinitrate, aspirin, and clopidogrel, and/or with glycoprotein IIb/IIIa inhibitors were compared with a control group of matched patients with STEMI without resolution, who were treated conventionally. The time interval from symptom onset to presentation at the emergency department of patients with TSTEMI was 1.7 +/- 1.3 hours, and to first recording of ST elevations, 1.5 +/- 1.4 hours. Symptoms and electrocardiographic changes fully resolved 1.2 +/- 0.8 hours later, 1 hour after aspirin and nitrate administration. Coronary angiography, performed 36 +/- 39 hours (median, 24 hours) from admission, demonstrated no obstructive lesion or single-vessel obstructive disease in 43 patients (70%). Primary coronary intervention was performed in 48 patients (77%), and 8 patients (13%) were referred to surgery. Left ventricular ejection fraction was within normal limits, and peak creatine kinase was mildly elevated. Patients with TSTEMI had less extensive coronary artery disease (P < .038), better thrombolysis in myocardial infarction flow on angiography (P < .01), lower peak creatine kinase level (P < .001), higher left ventricular ejection fraction (P < .0001), and lower likelihood to sustain a second additional coronary event after index admission (P = .024) than patients with STEMI. Transient STEMI was associated with less myocardial damage, less extensive coronary artery disease, higher thrombolysis in myocardial infarction flow grade in culprit artery, and better cardiac function. These data suggest that immediate intense medical therapy with an early invasive approach is an appropriate therapy in patients with TSTEMI.

Collateral pressure and flow in acute myocardial infarction with total coronary occlusion correlate with angiographic collateral grade and creatine kinase levels

BACKGROUND The validity of angiographic collateral grade according to the Rentrop classification during acute myocardial infarction (AMI) and its relation to flow in occluded coronary arteries before angioplasty have never been evaluated. METHODS We assessed the validity of the angiographic collateral grade according to Rentrop classification in relation to collateral pressure and flow beyond occluded coronary arteries during AMI. Pressure distal to coronary artery occlusions before balloon dilatation was measured in 111 patients undergoing angioplasty for AMI. We calculated the collateral flow index (CFI) and compared it to observed Rentrop grade and measured creatine kinase sum. RESULTS The values of pressure distal to coronary artery occlusions with respect to collateral grades 0 to 3 were 33 +/- 12, 37 +/- 13, 42 +/- 10, and 60 +/- 14 mm Hg (P < .0001). Overall CFI was 0.35 +/- 0.13 (median 0.33), with CFI values of 0.3 +/- 0.13, 0.33 +/- 0.13, 0.39 +/- 0.1, and 0.57 +/- 0.2 for collateral grades 0 to 3, respectively (P < .0001). Larger creatine kinase elevation (P < .016) and higher white blood cell count (P < .022) were recorded in the lowest tertile CFI compared with highest tertile CFI group; but no difference in the global, regional, or infarct-related regional left ventricular contraction was found. CONCLUSIONS These observations demonstrate that the Rentrop classification is valid in AMI patients with occluded coronary arteries and that collaterals are recruited acutely. These collaterals, whose pressure-derived CFI during AMI was shown for the first time to be higher than its value reported in chronic conditions, may limit the immediate myocardial damage or the systemic inflammatory response. No impact on global or regional cardiac contraction was detected in a population where most patients were treated early.

Pericardial Effusion due to Primary Malignant Pericardial Mesothelioma: A Common Finding but an Uncommon Cause

This case report describes a 37-year-old female who was admitted to our Emergency Department because of shortness of breath. On physical examination, she had dyspnea and tachycardia and blood pressure was 80/50 mmHg with a pulsus paradoxus of 22 mmHg. Neck veins were distended, heart sounds were distant, and dullness was found on both lung bases. Her chest X-ray revealed bilateral pleural effusion and cardiomegaly. On both computed tomography and echocardiography the heart was of normal size and a large pericardial effusion was noted. The echocardiogram showed signs of impending tamponade, so the patient underwent an emergent pericardiocentesis. No infectious etiology was found and she was assumed to have viral pericarditis and was treated accordingly. However, when the pericardial effusion recurred and empirical therapy for tuberculosis failed, a pericardial window was performed. A typical staining pattern for mesothelioma was found on her pericardial biopsy specimen. Since no other mesodermal tissue was affected, a diagnosis of primary malignant pericardial mesothelioma was made. Chemotherapy was not effective and she passed away a year after the diagnosis was made. This case highlights the difficulties in diagnosing this uncommon disease in patients that present with the common finding of pericardial effusion.