Background-The process of progression in coronary artery disease is unknown. Methods and Results-The subjects were 36 patients with 36 objective vessels with clinically significant progression of coronary artery disease (Ն15% per year) in whom 4 serial coronary arteriograms (CAGs) were performed at intervals of Ϸ4 months in a 1-year period. The degree of progression of percent stenosis between each of 2 serial CAGs was classified as marked (M: Ն15%), slight (S: 5% to 14%), and no progression (N: Ͻ5%). From the pattern of progression, the 36 vessels were classified as 14 type 1 vessels with marked progression (N3 N3 M in 13 vessels and S3 S3 M in 1 vessel) and 22 type 2 vessels without marked progression (S3 S3 S in 18 vessels, N3 S3 S in 4). Percent stenosis at the first, second, third, and final CAGs was 44Ϯ14%, 46Ϯ13%, 46Ϯ13%, and 88Ϯ10% (PϽ0.05 versus first CAG) in type 1 vessels and 44Ϯ11%, 50Ϯ9%, 59Ϯ9%, and 67Ϯ9% in type 2 vessels (PϽ0.05 for second, third, and final CAGs versus first CAG). Type 1 vessels featured the sudden appearance of severe stenosis due to marked progression, angina pectoris, or myocardial infarction (71%) and Ambrose type II eccentric lesions indicating plaque rupture or thrombi (57%). Type 2 vessels featured continuous slight progression of stenosis with smooth vessel walls; angina pectoris (14%) occurred when the percent stenosis reached a severe level. An increase in serum C-reactive protein was observed only in the type 2 vessel group, which suggests a relation between continuous slight progression and inflammatory change. Conclusions-Two types of stenosis progression provide a new insight into the mechanism of coronary artery disease.(Circulation. 1999;100:903-909.)
The appearance of marked progression and Ambrose's type II eccentric lesion on coronary angiograms 3 days before AMI suggests the presence of a considerable time from the onset of plaque rupture and/or thrombi until the onset of AMI. These features may be predictors of AMI. The concept provides new insight into the mechanism and prevention of human AMIs.
uidewire crossing is the most important component of a successful percutaneous coronary intervention (PCI) for chronic total occlusions (CTO). Several special guidewires, such as the Magnum wire, [1][2][3] Laser wire 4-6 and hydrophilic wire, 7 have been developed and favorable results have been reported. Other than these guidewires, some Japanese products, such as the Athlete, Miracle, and Conquest wires (Asahi Intecc, Seto, Japan), 8 are used in some countries and constitute a range of stiff products. In particular, the Conquest wire is a tapered spring coil wire with a very stiff tip (9 g) that gives good torque control and penetrating ability even in hard fibrous plaque. This type of guidewire may be the last choice for uncrossable, very old CTOs. 8 Although the Athlete wires will advance into a false lumen at the end of the procedure in unsuccessful cases, we can also use them to penetrate the flap to re-enter the true lumen as a second step.Coronary angiography is limited as a guide for guidewire crossing in PCI for CTOs. On the other hand, by showing the cross-sectional anatomy of the coronary vessels, intravascular ultrasound (IVUS) can provide information on the plaque morphology and distribution, 9 and the exact location of the guidewires within a coronary artery, discriminating a false lumen from the true lumen before guidewire crossing. We report here a novel application of IVUS for very old and hard CTOs (abrupt occlusion with a side branch in case 1 and bending occlusion with severe calcification in case 2) in which the use of very stiff guidewires caused dissections, decreasing the collateral flow. Case Reports Case 1: Side Branch MethodA 68-year-old Japanese man had experienced chest oppression on effort since May 2000. He visited hospital in July 2000, and coronary angiography revealed a CTO in the proximal segment of the large left circumflex coronary artery (LCX). There was no significant stenosis in the left anterior descending coronary artery (LAD) or the right coronary artery (RCA). His coronary arteries were left dominant. He had not had any episodes suggestive of acute myocardial infarction. Cardiac catheterization revealed left ventricular dysfunction and moderate mitral regurgitation. PCI for the CTO was unsuccessful at that time. He was treated medically and his condition improved. However, he complained of chest oppression on effort again in October 2001. We attempted to re-open the CTO of the LCX. The age of this CTO was unknown, but was thought to be more than 18 months, based on the angiographic record. We obtained the consent of the patient after fully explaining the efficacy and risks associated with our new technique using IVUS before the PCI.The occlusion was severely calcified and flush with the orifice of the vessel, tapering nicely into a large obtuse marginal artery (Fig 1a). A 10Fr JCL 4.0 with a side hole (Bright Chip, Cordis, Miami, FL, USA) was used in order to prepare for the possible use of a rotablator with a 2.5-mm burr. A 2.9Fr IVUS catheter (Ultracross, Boston Sci...
tandard 12-lead electrocardiography (ECG) is the simplest examination for diagnosing acute myocardial infarctions (AMI) because generally the infarct area and the segments with ST elevation correspond well with each other; that is, for AMI of the left anterior descending artery (LAD), right coronary artery (RCA) and left circumflex artery (LCX), the specificity of ST segment elevation is more than 90%. [1][2][3][4][5] Recording the ECG in AMI is very useful for making a prompt and precise diagnosis of the culprit artery, but for left main trunk (LMT) infarction, it is sometimes difficult to obtain the characteristic ECG findings because lethal arrhythmias, such as ventricular fibrillation, or atrioventricular block with hemodynamic compromise often occurs. These unstable hemodynamics can lead to cardiac arrest before the patient arrives at the hospital and thus a poor prognosis. Consequently, it is important to diagnose LMT infarction from the ECG on admission and institute coroCirculation Journal Vol.70, May 2006 nary interventions, such as mechanical assistance by an intra-aortic balloon pump, or surgical treatment without any delay.Some research has indicated that ST-segment elevation in lead aVR may indicate LMT infarction, 5-7 but to the best of our knowledge, the ECG features in LMT infarction have not been fully described. Methods Study PopulationThe records of 2,190 patients admitted to Gifu University Hospital and its referral hospitals with AMI from 1988 to 2004 were retrospectively collected from the data bank and 140 were enrolled and divided into 4 equal groups according to the location of the culprit artery: LMT, LAD, RCA (#3 and #4 AV) and LCX (#13 and #14). All patients immediately underwent coronary angiography and the extent of stenosis was evaluated according to American Heart Association classification. Exclusion criteria were (1) prior Q-wave myocardial infarction (MI), (2) prior coronary artery bypass graft operation, and (3) inability to identify the culprit lesion as a result of severe stenosis in 2 or 3 vessels. 2,3 A lesion was considered to be the culprit when it occluded or showed severe narrowing and ulceration with or without thrombus.Standard 12-lead surface ECG (paper speed: 25 mm/s, calibration: 1 mV =10 mm) was recorded as soon as possible after admission and various parameters (heart rate (HR),
AimsTo assess the involvement of sleep apnoea in nocturnal sudden cardiac death (SCD) by evaluating cardiac electrical instability using T-wave alternans (TWA), a risk marker for lethal cardiac arrhythmias, and severity of sleep apnoea in congestive heart failure (CHF) patients. Methods and resultsA total of 40 CHF patients simultaneously underwent overnight simplified respiratory polygraphy and 24 h continuous electrocardiography. Peak TWA during both daytime and nighttime were calculated by the modified moving average method. The patients were divided into two groups; 30 patients with daytime predominant TWA (whose peak TWA was higher during daytime than during nighttime) and 10 with nighttime predominant. Apnoeahypopnoea index (AHI) was significantly higher in patients with nighttime predominant TWA than in those with daytime predominant (35.9 + 8.1 vs. 23.9 + 14.4 events/h, P ¼ 0.02), and was an independent predictor of nighttime predominant TWA (odds ratio, 1.08; 95% confidence interval, 1.01-1.16; P ¼ 0.03). Moreover, peak TWA during the night was correlated positively with AHI (P , 0.001), and AHI was an independent determinant of nocturnal TWA value (r 2 ¼ 0.27, P ¼ 0.009). ConclusionIn CHF patients, sleep apnoea induces cardiac electrical instability manifested as TWA, reflecting increased risk of nocturnal SCD. Moreover, some CHF patients with sleep apnoea exhibit nighttime predominant TWA. Therefore, TWA should also be evaluated during the night.--
The study demonstrated for the first time that total spasm is a risk factor, independent of other factors, for cardiovascular events in patients with vasospastic angina. Treatment with benidipine showed a better prognosis than that with diltiazem.
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