Abstract Objective: To determine the effects of “prolonged” antiplatelet therapy (that is, given for one month or more) on “vascular events” (non-fatal myocardial infarctions, non-fatal strokes, or vascular deaths) in various categories of patients. Design: Overviews of 145 randomised trials of “prolonged” antiplatelet therapy versus control and 29 randomised comparisons between such antiplatelet regimens. Setting: Randomised trials that could have been available by March 1990. Subjects: Trials of antiplatelet therapy versus control included about 70 000 “high risk” patients (that is, with some vascular disease or other condition implying an increased risk of occlusive vascular disease) and 30 000 “low risk” subjects from the general population. Direct comparisons of different antiplatelet regimens involved about 10 000 high risk patients. Results: In each of four main high risk categories of patients antiplatelet therapy was definitely protective. The percentages of patients suffering a vascular event among those allocated antiplatelet therapy versus appropriately adjusted control percentages (and mean scheduled treatment durations and net absolute benefits) were: (a) among about 20 000 patients with acute myocardial infarction, 10% antiplatelet therapy v 14% control (one month benefit about 40 vascular events avoided per 1000 patients treated (2P< 0.00001)); (b) among about 20 000 patients with a past history of myocardial infarction, 13% antiplatelet therapy v 17% control (two year benefit about 40/1000 (2P<0.00001)); (c) among about 10 000 patients with a past history of stroke or transient ischaemic attack, 18% antiplatelet therapy v 22% control (three year benefit about 40/1000 (2P<0.00001)); (d) among about 20 000 patients with some other relevant medical history (unstable angina, stable angina, vascular surgery, angioplasty, atrial fibrillation, valvular disease, peripheral vascular disease, etc), 9% v 14% in 4000 patients with unstable angina (six month benefit about 50/1000 (2P<0.00001)) and 6% v 8% in 16 000 other high risk patients (one year benefit about 20/1000 (2P<0.00001)). Reductions in vascular events were about one quarter in each of these four main categories and were separately statistically significant in middle age and old age, in men and women, in hypertensive and normotensive patients, and in diabetic and non: diabetic patients. Taking all high risk patients together showed reductions of about one third in non-fatal myocardial infarction, about one third in non-fatal stroke, and about one sixth in vascular death (each 2P<0.00001). There was no evidence that non-vascular deaths were increased, so in each of the four main high risk categories overall mortality was significantly reduced. The most widely tested antiplatelet regimen was “medium dose” (75-325 mg/day) aspirin. Doses throughout this range seemed similarly effective (although in an acute emergency it might be prudent to use an initial dose of 160-325 mg rather than about 75 mg). There was no appreciable evidence that either a higher aspirin dose or any other antiplatelet regimen was more effective than medium dose aspirin in preventing vascular events. The optimal duration of treatment for patients with a past history of myocardial infarction, stroke, or transient ischaemic attack could not be determined directly because most trials lasted only one, two, or three years (average about two years). Nevertheless, there was significant (2P<0.00001) further benefit between the end of year 1 and the end of year 3, suggesting that longer treatment might well be more effective. Among low risk recipients of “primary prevention” a significant reduction of one third in non: fatal myocardial infarction was, however, accompanied by a non-significant increase in stroke. Furthermore, the absolute reduction in vascular events was much smaller than for high risk patients despite a much longer treatment period (4.4% antiplatelet therapy v 4.8% control; five year benefit only about four per 1000 patients treated) and was not significant (2P=0.09). Conclusions: Among a much wider range of patients at high risk of occlusive vascular disease than is currently treated routinely, some years of antiplatelet therapy - with aspirin 75-325 mg/day or some other antiplatelet regimen (provided there are no contraindications) - offers worthwhile protection against myocardial infarction, stroke, and death. Significant benefit is evident not only among patients with unstable angina, suspected acute myocardial infarction, or a past history of myocardial infarction, stroke, or transient ischaemic attack, but also among many other categories of high risk patients (such as those having vascular procedures and those with stable angina or peripheral vascular disease). There is as yet, however, no clear evidence on the balance of risks and benefits of antiplatelet therapy in primary prevention among low risk subjects.

Collaborative overview of randomized trials of antiplatelet therapy .1. prevention of death, myocardial-infarction, and stroke by prolonged antiplatelet therapy in various categories of patients

Coronary artery anomalies were found in 1,686 patients (13% incidence) undergoing coronary arteriography at the Cleveland Clinic Foundation from 1960 to 1988 Of the 1,686 patients, 1,461 (87%) had anomalies of origin and distribution, and 225 (13%) had coronary artery fistulae Most coronary anomalies did not result in signs, symptoms, or complications, and usually were discovered as incidental findings at the time of catheterization Eighty-one percent were “benign” anomalies: (1) separate origin of the left anerior descending and circumflex from the left sinus of Valsalva; (2) ectopic origin of the circumflex from the right sinus of Valsalva; (3) ectopic coronary origin from the posterior sinus of Valsalva; (4) anomalous coronary origin from the ascending aorta; (5) absent circumflex; (6) intercoronary communications; and (7) small coronary artery fistulae Other anomalies may be associated with potentially serious sequelae such as angina pectoris, myocardial infarction, syncope, cardiac arrhythmias, congestive heart failure, or sudden death Potentially serious anomalies include: (1) ectopic coronary origin from the pulmonary artery; (2) ectopic coronary origin from the opposite aortic sinus; (3) single coronary artery; and (4) large coronary fistulae Coronary artery anomalies require accurate recognition, and at times, surgical correction

https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccd.1810210110

Coronary artery anomalies in 126,595 patients undergoing coronary arteriography.

Background Coronary calcium identified by electron-beam computed tomography (EBCT) correlates poorly with luminal atherosclerotic narrowing, but calcium, an intimate part of coronary plaque, may be more directly related to atheromatous plaque area. Methods and Results Thirty-eight coronary arteries from 13 autopsy hearts were dissected, straightened, and scanned with EBCT in 3-mm contiguous increments. Coronary calcium area was defined as one or more pixels with a density >130 Hounsfield units (0.18 mm 2 /pixel). Each artery was divided into corresponding 3-mm segments, representative histological sections were stained, and atherosclerotic plaque area per segment (mm 2 ) was quantified. Coronary artery calcium and coronary artery plaque areas were correlated for the hearts as a whole, for individual coronary arteries, and for individual coronary artery segments. The sums of histological plaque areas versus the sums of calcium areas were highly correlated for each heart and for each coronary artery. However, coronary plaque area was on the order of five times greater than calcium area. Furthermore, minimal diffuse segmental coronary plaque could be present despite the absence of coronary calcium detectable by EBCT. Conclusions This histopathologic study confirms an intimate relation between whole heart, coronary artery, and segmental coronary atherosclerotic plaque area and EBCT coronary calcium area but suggests that there is a threshold value for plaque area below which coronary calcium is either absent or not detectable by this methodology.

Coronary Artery Calcium Area by Electron-Beam Computed Tomography and Coronary Atherosclerotic Plaque Area A Histopathologic Correlative Study

To assess visual interpretation of the coronary arteriogram as a means of predicting the physiologic effects of coronary obstructions in human beings, we compared caliper measurements of the degree of coronary stenosis with the reactive hyperemic response of coronary flow velocity studied with a Doppler technique at operation, after 20 seconds of coronary arterial occlusion. In 39 patients (44 vessels) with isolated, discrete coronary lesions varying in severity from 10 to 95 per cent stenosis, measurement of the percentage of stenosis from coronary angiograms was not significantly correlated (r = -0.25) with the reactive hyperemic response. Results were the same for obstructions in the left anterior descending, diagonal, and right coronary arteries. Underestimation of lesion severity occurred in 95 per cent of vessels with >60 per cent stenosis of the diameter by arteriography. Both overestimation and underestimation of lesions with <60 per cent stenosis were common. These results, together with...

Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis

/pdf/diagnosis-and-management-of-aortic-dissection-ol93ou3jw4.pdf

Diagnosis and management of aortic dissection

Four experienced coronary angiographers (two radiologists and two cardiologists) independently assessed the location and degree of coronary artery stenosis, and the location and degree of left ventricular wall motion abnormalities in 20 coronary angiograms. Marked interobserver variability was noted in quantifying percent coronary artery stenosis and degree of left ventricular wall motion abnormalities. For example, in only 13/20 (65%) of the coronary angiograms did all observers agree about the significance of a stenosis (defined as greater than 50% in diameter luminal narrowing) in the proximal or mid left anterior descending coronary artery. In 3/20 (15%) angiograms there was disagreement by at least one observer about the significance of lesions noted in the main left coronary artery. The ventricle was divided into five segments and the degree of wall motion abnormality graded into six categories of increasing severity from normal to dyskinesis. There was a 42% mean disagreement among all four observers where a disagreement between observers was defined as any difference in grading wall motion abnormalities. Interobserver variability reveals a significant limitation of coronary angiography.

Interobserver variability in coronary angiography.

The effect of antithrombotic therapy on patency rates of saphenous vein coronary artery bypass grafts

UNLABELLED Subclavian crush syndrome, described with pacemaker leads implanted via subclavian puncture, may occur when conductor fractures and insulation breaches develop by compression of a lead between the first rib and clavicle. We reviewed our experience in 164 patients who underwent intended implantation of transvenous defibrillator systems to determine the clinical relevance of subclavian crush syndrome in defibrillator patients. Venous access was obtained via subclavian puncture in 114 patients (70%) and via cephalic cut-down in 50 patients (30%). Nonthoracotomy lead systems, with or without subcutaneous patch, were successfully implanted in 131 of 164 patients (79.9%). Thoracotomy was required in 32 patients (19.5%) and subxiphoid patch in 1 patient (0.6%). Over a mean of 12.9 months (range 1-62 months), 3 patients (1.8%) required revision of the rate sensing lead/coil or superior vena cava coil after development of lead compression fractures in the region of the clavicle and first rib. In all 3 patients the leads had been implanted via subclavian puncture (2.6% of patients in whom the subclavian technique was utilized). Two patients presented with spurious shocks. One patient was asymptomatic. CONCLUSIONS When venous access is obtained via subclavian puncture, subclavian crush syndrome may develop in patients with transvenous defibrillator systems. Patients may be asymptomatic and lead fractures may go unrecognized. When implanting transvenous defibrillator systems, strong consideration should be given to obtaining venous access primarily via the cephalic cut-down technique.

Subclavian Crush Syndrome Complicating Transvenous Cardioverter Defibrillator Systems

The relation between the extent of angiographic coronary artery disease and the presence of chronic heart failure in patients with coronary artery disease has not hitherto been clearly elucidated. In the present study clinical, ventriculographic, and coronary arteriographic features are compared in 84 patients with coronary artery disease. The extent of coronary disease is measured by the angiographicjeopardy score, which expresses how many of six coronary arterial segments are jeopardised by significant (> 70% estimated luminal area reduction) proximal stenoses. Each jeopardised segment is counted as 2 points. Thirty of the 84 patients had clinical evidence of chronic heart failure, all of whom were classified as having a cardiomyopathic syndrome caused by coronary artery disease since all had significant reduction of the left ventricular ejection fraction (<0-48) because of multiple and widespread left ventricular wall motion abnormalities. There were no patients in this study with chronic heart failure from other causes (e.g. isolated ventricular aneurysm). The mean jeopardy score in the patients with cardiomyopathy was much higher than in the patients without cardiomyopathy (10-7±0-4 vs 5-3±0-6, P<0-01), and all patients with cardiomyopathy had a jeopardy score .8. Distal coronary artery disease was unrelated to the presence or absence of cardiomyopathy (0.5± 0 2 vs 0 4 ± 0 2 diseased distal vessels per patient). Cardiomyopathy was strongly associated with the occurrence of multiple myocardial infarcts (1.9±0.3 myocardial infarcts per patient) in the group with cardiomyopathy and 0-9±0-2 myocardial infarcts per patient in the group without it; 19 of 30 (64%) patients with cardiomyopathy had .2 myocardial infarcts, whereas 11 of 54 (20%) without had >2 myocardial infarcts (P<0-001). Thefindings of this study, that cardiomyopathy due to coronary artery disease is specifically related to the extent ofproximal coronary artery disease and to the occurrence of multiple myocardial infarcts, constitute reasonsfor distinguishing this cardiomyopathic syndromefrom the several other causes of chronic heart failure in coronary artery disease. The angiographic scoring system used here, which more precisely relates the extent of coronary disease to the extent of left ventricle involved, was a stronger predictor of the presence or absence of the cardiomyopathic syndrome than the 1, 2, 3-vessel disease notation.

https://heart.bmj.com/content/heartjnl/39/7/733.full.pdf

Cardiomyopathic syndrome due to coronary artery disease. I: Relation to angiographic extent of coronary disease and to remote myocardial infarction.

THE chordae tendineae serve an essential anchoring function in the mechanics of mitral-valve closure during ventricular systole. Rupture of one or more of these fibrous structures usually leads to mitral regurgitation, the severity of which is related to the location and number of chordae tendineae involved1 as well as the presence of prior disease of the mitral valve itself. Although active bacterial endocarditis was probably the major cause of ruptured chordae tendineae in the preantibiotic era,2 rheumatic mitral valvulitis, often with healed bacterial endocarditis, appears to be the most common etiology at present.3 4 5 However, a significant number of cases have . . .

Harthorne Jw

Papers

Interobserver variability in coronary angiography.

The effect of antithrombotic therapy on patency rates of saphenous vein coronary artery bypass grafts

Subclavian Crush Syndrome Complicating Transvenous Cardioverter Defibrillator Systems

Cardiomyopathic syndrome due to coronary artery disease. I: Relation to angiographic extent of coronary disease and to remote myocardial infarction.

Diagnosis and Surgical Treatment of Mitral Regurgitation Secondary to Ruptured Chordae Tendineae