Coronary artery ectasia: is it associated with myocardial ischaemia and infarction?

Coronary artery ectasia is an uncommon finding during coronary angiography. There may be associated stenoses of the affected arteries. We report three cases, which illustrate that ectasia, in the absence of obstructive disease, can result in myocardial ischaemia and infarction.

Association of patient delay with symptoms, cardiac enzymes, and outcome in acute myocardial infarction.

The delay between the onset of symptoms and the call for help is the longest single component of the time taken for patients with acute myocardial infarction to come under coronary care and receive thrombolytic therapy. In order to investigate factors influencing patient delay, visual analogue scores for pain, shortness of breath, and anxiety were obtained retrospectively from 250 patients with acute myocardial infarction, for the time of onset of symptoms, and for the time of the call for help. The predominant symptom was chest pain, followed by anxiety and breathlessness. Although all symptoms increased in severity after their onset, the initiation of a call was largely unexplained in terms of worsening symptoms. Patient delay had a skewed distribution with modal, median and mean values of up to 1 h, 1.5 h, and 11 h respectively. Patient delay was negatively correlated with the pain score at the time of calling, but most of the variance of patient delay could not be explained in terms of symptom scores. However, patient delay was independently and negatively related to maximum serum aspartate aminotransferase. During acute myocardial infarction, patients with higher cardiac enzyme levels experience more pain and delay less. This tendency for patients with more severe infarction and a greater risk of death to call for help sooner is an added reason for administering thrombolytic treatment at the first opportunity: those patients who call early have most to gain from prompt therapy.

Long-term prognosis after resuscitation from primary ventricular fibrillation complicating acute transmural myocardial infarction in the north east of Scotland.

The aim of this study is to determine the long-term prognosis of patients successfully resuscitated from primary ventricular fibrillation in the acute phase of transmural myocardial infarction and to identify predictors of mortality. Details of 75 consecutive patients between October 1971 and May 1981 were reviewed in October 1985. The cumulative survival rates at one year, two year, five year and 10 year were 84%, 77% 67% and 40.5% respectively with a median survival time of 8.7 years. Univariate and Cox survival analyses were used to determine predictors of mortality. Only the age of the patient at the time of infarction was found to be highly significant with a greatly increased mortality rate in the older age group (p less than 0.001). The sex, site of infarction (anterior or inferior) and time of entry in the study did not significantly influence long-term prognosis.

Reversibility of primary pulmonary hypertension during six years of treatment with oral diazoxide.

A 32 year old woman presented with a syncopal attack and dyspnoea on exertion. A diagnosis of primary pulmonary hypertension was confirmed by clinical examination, cardiac catheterisation, and pulmonary angiography. Her symptoms resolved completely with oral diazoxide and the pulmonary arterial pressure was reduced to normal levels over a period of six years. When diazoxide was discontinued on two separate occasions pulmonary hypertension recurred. This demonstrated the continued presence of the underlying stimulus for vasoconstriction.

The effect of thrombolytic therapy with anisoylated plasminogen streptokinase activator complex on the indicators of myocardial salvage.

The role of anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction, in effecting thrombolysis, in limiting infarct size and in preserving myocardial function, was assessed by comparing APSAC and placebo in a double-blind, randomised trial. Between October 1984 and April 1985, 43 patients (mean age 57.3 years) with evolving infarctions (19 anterior/24 inferior) were randomised. All patients received treatment within 3 hours of the onset of pain. Patients over 70 years of age or with contraindications to thrombolytic therapy were excluded. Response to therapy was assessed by comparing reductions in summated ECG R wave amplitude and changes in QRS score at 24 hours and 7 days in the leads with ST abnormalities on admission. Radionuclide ejection fractions (EF) were performed 2 to 6 months after infarction. Evidence of successful reperfusion was based on non-invasive parameters. Mean time to peak cardiac enzyme release was shorter in the active treatment group, indicating effective thrombolysis (11.5 hours vs 17.6 hours; p less than 0.01). No differences were found in R wave reduction or QRS score at either 24 hours or 7 days, between active and placebo groups in total or when divided by infarct site. No difference was seen between the EFs of the groups in total or between inferior infarct groups. The mean EF of the treated anterior group was higher than that of the untreated group (p less than 0.05). Successful thrombolysis was seen in the actively treated group. Evidence of myocardial salvage and preservation was seen among treated patients with anterior infarcts only.

The results of coronary arteriography in young men after myocardial infarction in north-east Scotland.

The case records of 50 consecutive male patients aged 40 years or under who were investigated by selective coronary arteriography after myocardial infarction were reviewed. Fourteen patients had normal coronary vessels and 36 patients had significant occlusive disease. Eighteen were considered to be in need of surgical treatment. The features of myocardial infarction on the ECG were less marked in the group of patients with normal coronary arteriograms. Many of these patients were asymptomatic and had complete resolution of the ECG changes. As well as having normal coronary arteries, many also had normal left ventricular angiograms. Cigarette smoking was very common in the whole group, 86 per cent of patients being moderately heavy cigarette smokers. Five of the 14 patients in the 'non-occlusive' group were non-smokers and only two of the 36 patients in the 'occlusive' group were non-smokers (P less than 0.01). The fasting serum cholesterol was significantly lower in the 'non-occlusive' group than in the 'occlusive' group. There was no significant difference between the two groups regarding blood pressure, family history of ischaemic heart disease, obesity or alcohol consumption. There was, however, a high incidence of heavy alcohol consumption amongst patients who subsequently required coronary artery surgery. Many of the patients in the 'non-occlusive' group were considered to have had smaller, more localised myocardial infarctions and a lesser degree of coronary disease which may not be detected by coronary arteriography. Others, with more widespread cardiac damage, could be explained on the basis of thrombosis and subsequent recanalisation.

Electrocardiogram of pure left ventricular hypertrophy and its differentiation from lateral ischaemia.

In routine reporting of electrocardiograms, a frequent problem is presented by the presence of repolarisation abnormalities (ST depression and/or T wave inversion) in the lateral leads without the accepted QRS voltage criterion of left ventricular hypertrophy. To help resolve this problem, the electrocardiograms of 41 patients with severe aortic stenosis who had no evidence of coronary disease were compared with the electrocardiograms of 20 patients with lateral myocardial infarction who had no clinical evidence of left ventricular hypertrophy. Nine of the patients with aortic stenosis were found to show repolarisation abnormalities in the lateral leads without the standard voltage criterion of left ventricular hypertrophy. The repolarisation pattern of aortic stenosis could frequently be distinguished from that of coronary disease by the presence of one or more of the following five features: depression of the J point, asymmetry of the T wave with rapid return to the baseline, terminal positivity of the T wave ("over-shoot"), T inversion in V6 greater than 3 mm, and T inversion greater in V6 than in V4.

Coronary heart disease in North-East Scotland a study of genetic and environmental variation in serum lipoproteins and other variables.

1. Serum lipoprotein concentrations and other variables such as relative weight, skinfold thickness, blood pressure, serum glucose, uric acid, fibrinogen smoking habits, etc. have been recorded on about 700 persons, including about 200 survivors of myocardial infarction under age 50 years, 250 of their relatives and 250 unrelated controls. 2. Elevated levels of VLDL and LDL are several times more frequent in survivors of infarction than in controls. 3. Cigarette smoking is associated with 20 to 30 per cent increase in VLDL. 4. Relative weight and skinfold thickness together account for a quarter of the variance of VLDL in men, 9 per cent in women. 5. LDL and HDL are uncorrelated; there is a low, consistently negative correlation between HDL and VLDL and IDL. 6. Parent-offspring regression and sib correlations indicate high, intermediate and low heritability for respectively HDL, LDL and VLDL. First degree relatives of survivors of infarction have levels of VLDL, IDL and LDL but not HDL.

Frequency and significance of conduction defects in acute myocardial infarction.

The frequency of intraventricular conduction defects was determined in 556 consecutive patients with proven acute myocardial infarction. Complete left bundle branch block was present in 23 patients and carried a high mortality rate (61 per cent). Complete right buldle branch block was the rarest defect to be seen in isolation (8 patients) and carried a lower mortality rate (38%). Lone left anterior hemiblock was present in 72 patients and was associated with a low mortality rate (13 per cent); left posterior hemiblock occurred in 32 patients (mortality rate 19 per cent). In a further 59 patients right bundle branch block with left anterior or posterior hemiblock in addition was present and these patients had a high mortality rate which was greater than isolated right bundle branch block or hemiblock alone. Complete atrioventricular block developed in 51 patients, 26 of whom had prior evidence of intraventricular conduction defect. Despite the use of temporary transvenous pacing, mortality in patients who developed complete heart block was significantly increased whether or not an intraventricular conduction defect was already present. The significance of these findings for the management of patients with myocardial infarction is discussed.

Controlled trial of oxygen in uncomplicated myocardial infarction.

Two-hundred consecutive patients thought to have suffered a myocardial infarction were admitted to a randomised, double-blind controlled trial of oxygen or air administered by MC mask throughout the first 24 hours in hospital. Forty-three patients in whom myocardial infarction was not subsequently confirmed were excluded from the analysis. The remaining air and oxygen groups were comparable except for a significantly higher PaO2 and serum aspartate aminotransferase level in the oxygen group. There was no significant difference in mortality, incidence of arrhythmias, use of analgesics, or systolic time intervals between the two groups, although a higher incidence of sinus tachycardia was found in those given oxygen. There appears to be no evidence of benefit from the routine administration of oxygen in uncomplicated myocardial infarction.