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STEMI patients admitted urgently to the hospital but experience early complete resolution of both ischemic symptoms and ST-elevations on the electrocardiogram are diagnosed as transient STEMI (TSTEMI). Current evidence indicates that primary intervention is plausible but in certain circumstances intervention can be delayed. We sought to examine whether there is a time limit to such a delay that may affect long-term outcome. Study population included prospectively admitted TSTEMI patients whose demographics, pertinent medical history, and clinical and angiographic features were recorded. Study patients were divided by the median time interval from admission to intervention and their characteristics and long-term survival were compared. Study population comprised 260 consecutive patients (age: 57±10 years, men: 84%) diagnosed as TSTEMI who were included from January 2000 to June 2019, which represent 6% of all STEMI patients. Coronary angiography was performed in 254 patients. The median time interval from admission to angiography was 17 hours (IQR: 7.2 to 38.7 hours). Early (17 hours from admission) and late (17 hours from admission) study groups were comparable. One patient died during admission and 41 throughout the long follow-up period of 8.5 ± 5.2 years (median: 8.2 years, IQR: 3.4 to 13.1). Mortality of early-treated TSTEMI patients (11.2%) was significantly lower than of the late-treated patients (21.6%, p0.04). The Kaplan-Meier curve demonstrated a clear tendency toward improved survival in early-treated TSTEMI patients (p0.09). In conclusion, the present data suggest that TSTEMI patients should be treated, if not by primary coronary intervention, then at least within 17 hours from admission to achieve better long-term outcome.

It is frequently difficult to differentiate between perimyocarditis and acute myocardial infarction (AMI). Diagnosis is usually established by excluding obstructive coronary disease. The primary process in perimyocarditis is inflammation, associated with high C-reactive protein (CRP) and low

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.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.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.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.

Acute heart failure (AHF) evolves through two phases. In the first phase, there is interstitial congestion with no clinical sign of edema (preclinical phase); the second, during which lung alveoli begin to fill with fluid, manifests as clinically overt alveolar edema. Treatment of AHF at its preclinical phase can alleviate its clinical impact. Presently, there is no technique that detects the interstitial phase of AHF. We used a device based on a new method of lung bioimpedance measurement. The device measures internal thoracic impedance (ITI), which nearly equals inherent lung bioimpedance. This method can detect small changes in lung fluid that occur during the interstitial stage of AHF.The objective of this study was to assess the feasibility and efficacy of the said new method in detecting preclinical AHF.Internal thoracic impedance and pertinent clinical parameters were monitored for 72 h in 403 patients hospitalized for an acute coronary syndrome without evidence of AHF at study entry.Seventy patients developed AHF during monitoring. Internal thoracic impedance decreased in these patients by 16.4% (95% CI=-12.2% to -20.6%; P.0001) from the baseline level at 44+/-15.1 min prior to the onset of lung rales. The other 333 patients had no clinical sign of AHF, and their ITI declined only by 4.5% (95% CI=2.5% to -11.5%; P=.3) compared with the baseline level.The new method for ITI measurement is sufficiently sensitive in detecting AHF at its preclinical stage. An ITI decrease of more than 12% heralds the appearance of clinically overt AHF and, thus, allows earlier therapy.

One hundred thirty-nine patients who underwent transesophageal echocardiographic studies were grouped by their maximal left atrial (LA) volumes, and their stroke volumes, emptying fractions, and fractional shortening were calculated. In large atria, an inverse relation was found between further increases in LA volume and LA function, determined by emptying fractions and fractional shortening.

Background: Five to 15% of the population have allergy to nickel, chromium, or molybdenum, which is a potential cause for in-stent restenosis. The Titan stent is made of stainless steel and is coated with titanium-nitride oxide (TiNOX), which completely prevents the discharge of metal elements. We performed a real-life multicenter registry to assess the short- and long-term characteristics of the Titan stent. Methods and results: A total of 103 Titan stents was implanted in 100 patients. Patients were 61.4F12.6 years old (81 men). Risk factors included hypercholesterolemia (63%), hypertension (53%), diabetes mellitus (DM; 35%), and current smoking (23%). Indications for PCI (percutaneous coronary intervention) were acute coronary syndromes (ACS) in 68% [acute ST elevation myocardial infarction (MI) in 8%], stable AP (angina pectoris) in 25%, and silent ischemia in 7% of the patients. Fifty-two percent of the treated lesions were of Type B2 or C. Lesion length was 14.3F2.9 mm and stent diameter was 3.06F0.36 mm. Indications for stenting were prevention of restenosis in 66%, residual stenosis in 33%, dissection in 13%, acute MI in 13%, and in-stent restenosis in 7% of the patients. Procedural success was 100%, with no complications. At 30 days, there were no major adverse cardiac events (MACE), including death, MI, and revascularization. At 180 days, only three patients had TVR (target vessel revascularization); two had TLR (target lesion revascularization) (one PCI and one CABG [coronary artery bypass grafting]), and one patient had a new narrowing proximal to the stent and underwent CABG due to multivessel disease. Conclusions: The Titan stent has a remarkable safety profile in high-risk patients and complex coronary lesions and excellent short- and long-term outcome with a very low clinical TLR rate. D 2005 Elsevier Inc. All rights reserved.

Background. The major limitation of coronary stenting is restenosis due to exaggerated neointimal thickening. We evaluated a positron-emitting V48 nitinol stent in a porcine coronary model of restenosis. Methods and Results. Pigs (n = 16) received a control nonradioactive and a V48 stent (1.5 or 10.6 μCi) randomized to the left anterior descending artery (LAD) and right coronary artery (RCA). Histology, morphometric variables, and strut injury scores were evaluated after 32 days. Peristrut fibrinoid deposits were greater in the high-dose group (p < 0.0001). Control stent area stenosis (AS) and mean neointimal thickness (NIT) correlated with injury (r = 0.81 and 0.79, respectively). Higher-dose stents reduced AS by 20% (0.57 ± 0.13 vs. 0.71 ± 0.16; p = 0.029) and mean NIT by 35% (0.44 ± 0.16 vs. 0.71 ± 0.24mm; p = 0.001) compared with controls. Lower-dose 1.5-μCi stents did not differ from controls. NIT over individual struts was reduced in the high-dose group compared with controls by 0.18 mm for grade 1 injury, 0.31 mm for grade 2, and 0.38 mm for grade 3 (p < 0.02 for all comparisons). Conclusions. 1.5-μCi V48 nitinol stents did not influence vessel histology or restenotic parameters in pig coronary arteries. In contrast, 10.6-μCi stents created a distinctive histological picture consisting of increased fibrinoid deposits on the neointimal-facing side of the struts without cellular organization. Higher dose radioactive stents significantly reduced AS and mean NIT. The reduction in neointimal thickening was greatest when the depth of strut penetration into the vascular wall was most severe.