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Patients with suspected acute coronary syndrome are commonly assessed by acute physicians on arrival in hospital. Although most will recognise the typical ECG features of ST elevation myocardial infarction, the significance of ST elevation in lead aVR may not always be appreciated. This case series describes 6 cases in which this ECG abnormality was the predominant feature in patients whose subsequent angiogram revealed severe acute left main coronary artery disease. The importance of early referral of such patients to a centre in which percutaneous coronary intervention can be performed, is discussed.

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Propionibacterium acnes is a constituent of the normal skin flora. It has been described as causing infection on prosthetic valves but very rarely on native valves. We describe a case of aggressive P. acnes endocarditis in a healthy 36-y-old man which infected a native aortic valve and was complicated by an aortic root abscess and review the literature.

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Angiotensin II (Ang II) exerts an inhibitory action on vagal activity in animals and may also facilitate sympathetic activity. The object of this study was to compare autonomic activity resulting from equivalent steady-state baroreflex activation during intravenous Ang II infusion with that resulting from a control infusion of phenylephrine. Eight healthy subjects aged 22 to 34 years were studied in a single-blind, randomized, prospective crossover study. Autonomic activity was determined by computer analysis of RR interval variability in the time and frequency domains. Despite equal experimental hypertension with Ang II and phenylephrine infusion, at peak infusion rates the mean RR interval was significantly shorter with Ang II (983 +/- 179 milliseconds; mean +/- SD) than with phenylephrine (1265 +/- 187 milliseconds, P < .01). The variability of RR intervals was not significantly different, but the variability (median interquartile difference) of RR interval successive differences was significantly lower with Ang II (66 milliseconds) than with phenylephrine (104 milliseconds, P < .02). Power spectral analysis revealed the power of the 0.25-Hz component in normalized units to be significantly smaller during Ang II infusion (20.5 +/- 12.7 U) than during phenylephrine (38.2 +/- 14.7 U, P < .05), whereas the power of the 0.1-Hz component was significantly greater during Ang II infusion (67.8 +/- 17.1 U) than phenylephrine (38.8 +/- 20.3 U, P < .05). Measures of vagal modulation of heart rate were significantly attenuated, and sympathetic modulation appeared to be increased during Ang II infusion compared with control phenylephrine infusions. These observations may underlie reports of increased vagal activity during angiotensin-converting enzyme inhibitor therapy.

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Successful dual chamber pacing was achieved by implanting permanent pacemaker leads using an extra-peritoneal approach to the inferior vena cava in a 48-year-old patient with a single ventricle, transposition of the great vessels, and a right atrial pulmonary artery shunt (Glenn's procedure). The pacemaker generator was implanted into a subcutaneous pocket in the anterior abdominal wall.

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The effect of quinapril on blood pressure (BP), heart rate (HR) and their variabilities in 12 patients with severe congestive heart failure (New York Heart Association class III and IV) was assessed using ambulatory electrocardiographic and intraarterial monitoring. Mean +/- standard deviation daytime BP was 122/75 +/- 20/15 mm Hg at baseline and 113/70 +/- 13/16 mm Hg after 16 weeks of therapy with quinapril (p greater than 0.05 for systolic and diastolic BP); mean nighttime BP was 114/69 +/- 19/14 mm Hg at baseline and 107/69 +/- 15/14 mm Hg with quinapril (p greater than 0.05 for systolic and diastolic BP). Mean daytime HR was unchanged but nighttime HR was reduced from 77 +/- 11 to 71 +/- 10 beats/min, p = 0.02. HR variability (difference between the 75th and 25th percentiles of the frequency distribution of RR intervals) increased from 91 +/- 34 to 134 +/- 47 ms, p = 0.008. The variability of successive differences between RR intervals also increased significantly (75th to 25th percentile = 17 +/- 4 ms at baseline and 31 +/- 26 ms with quinapril, p = 0.02). Long-term quinapril caused clinically unimportant decreases in BP in patients with severe congestive heart failure. An increase in vagal activity caused by the reduction in circulating angiotensin II may account for the effect of converting enzyme inhibition on HR and its variability.

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A validation study of the Takeda TM-2420 ambulatory blood pressure recorder was performed on 10 subjects using the Oxford ambulatory intra-arterial recording apparatus during unrestricted activity. Electronic linkage of the two recorders ensured simultaneous blood pressure readings, taken from opposite arms. Although there was close approximation of intra-arterial and automated sphygmomanometric recordings over the range of blood pressure encountered in this study, there was a wide scatter of points and a tendency for the machine to underestimate systolic pressure by more than 15 mm Hg in the hypertensive range (systolic blood pressure more than 160 mm Hg) was detected. These findings suggest that automated recording of blood pressure during unrestricted activity may have a proportion of artifactual readings. Although simultaneous intra-arterial blood pressure recording may not be appropriate for widespread use in device validation, this study illustrated some potential disadvantages of the current validation recommendations, namely, the absence of assessment of device accuracy during unrestricted and ambulatory activity.

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Myocardial infarction as a result of injury to the coronary arteries is a rare complication of non-penetrating chest trauma. We report a case of fatal inferior wall myocardial infarction following traumatic injury to the right coronary artery, complicated by atrioventricular dissociation, in a patient with a combination of hypertrophic cardiomyopathy and non-occlusive coronary artery disease.

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1. The effects of posture and exercise on the relationship between low-level urinary albumin excretion (microalbuminuria) and blood pressure was investigated in two groups of non-diabetic patients at increased cardiovascular risk: 21 otherwise healthy patients with untreated essential hypertension (blood pressure greater than 160/90 mmHg), and 14 age-matched patients with blood pressure at presentation within the normotensive range (less than 160/90 mmHg) attending a cardiovascular clinic for assessment of chest pain. 2. A significant linear relationship between logarithmically transformed 'spot' urinary albumin/creatinine ratio and simultaneous clinic blood pressure existed when data from both groups of patients were analysed (r = 0.58, P less than 0.05). The relationship between the scatter plot of blood pressure and the albumin/creatinine ratio appeared most marked when the mean blood pressure exceeded 120 mmHg. 3. In patients with essential hypertension, clinic systolic blood pressure was related to the albumin/creatinine ratio in simultaneous 'spot' urine samples (r = 0.69, P less than 0.05) and also to the albumin/creatinine ratio in early-morning urine samples (r = 0.51, P less than 0.05). However, the relationship between clinic blood pressure and simultaneous 'spot' urinary albumin/creatinine ratio in the patients with chest pain did not achieve significance when analysed independently. 4. Hourly averaged ambulatory intra-arterial blood pressure was recorded in four of the patients with essential hypertension during normal daytime activity, and a significant correlation with the simultaneous hourly daytime urinary albumin/creatinine ratio was found (r = 0.65, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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The effects of monotherapy with the angiotensin converting enzyme inhibitor benazepril (10 mg once daily) on cardiovascular baroreceptor reflexes were determined in 10 patients with essential hypertension using a randomized, double-blind, placebo-controlled, cross-over protocol. Early sino-aortic baroreceptor/heart rate reflex resetting was apparent with acute treatment; this effect persisted throughout the active treatment period. Changes in baroreflex sensitivity did not appear to mediate the hypotensive effect of benazepril.

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Transient electrocardiographic changes resembling acute myocardial infarction, with Q-waves and ST-segment elevation, have been reported in a variety of clinical situations in which evidence for acute myocardial necrosis was not apparent. Such electrocardiographic changes resolved to normal within minutes. We report a case in which exercise testing induced a painless reversible electrocardiographic abnormality identical to acute anterior myocardial infarction, and subsequent angiography revealed a severe stenosis in the proximal left coronary artery. We suggest that patients presenting with this type of electrocardiographic exercise response should proceed to urgent coronary angiography.

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The effect of xamoterol on the orthostatic hypotension associated with Shy-Drager syndrome was investigated in three patients. Intra-arterial blood pressure was measured during a control period and during treatment with xamoterol, both in a cardiovascular investigation laboratory and for 24 h of unrestricted activity using portable apparatus. Xamoterol lessened the total number of symptomatic episodes of orthostatic hypotension by 67 per cent. Average untreated 24-h intra-arterial blood pressure was 132/78 mmHg; during treatment with xamoterol it rose to 138/90 mmHg. However episodes of severe hypertension (defined as a systolic intra-arterial blood pressure above 200 mmHg) were more frequent with xamoterol. Although xamoterol attenuated orthostatic hypotension, careful monitoring of ambulatory blood pressure may be necessary, particularly at the start of treatment, because of the development of severe supine hypertension. Intravenous test doses of xamoterol did not predict either the attenuation of orthostatic hypotension or the development of supine hypertension in all patients.

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1. There is a biphasic flow response measured plethysmographically after release of prolonged venous occlusion of the forearm. 2. The response consists of an early, vasodilatory, increase in flow and is followed by a decrease in flow relative to control, thought to be mediated by myogenic contraction of resistance vessels. 3. Methodological constraints with the technique of forearm plethysmography have to date precluded an individual beat-by-beat examination of this response, in particular for resolving the question of the immediate flow pattern after release of venous occlusion. It has been suggested by Caro, Foley & Sudlow [Journal of Physiology (London) (1970), 207, 257-269] that there is a delay of up to five systolic beats before vasodilatation takes place, leading to their suggestion that the vasodilatation is passive and secondary to an increased flow through emptied capacitance vessels. 4. The introduction of peripheral Doppler techniques has led us to re-examine this response in an attempt to define short-term resistance vessel behaviour on a beat-by-beat basis. 5. Our data confirmed the hypothesis of Caro, Foley & Sudlow [Journal of Physiology (London) (1970), 207, 257-269] that there is a constant and definite latency preceding the onset of vasodilatory flow, as reflected by changes in Doppler velocities.

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A panel of two physicians and two ophthalmologists examined 25 patients with untreated essential hypertension by direct ophthalmoscopy and assessment of fundal photographs; daytime ambulatory sphygmomanometric blood pressure monitoring, estimation of left ventricular mass by electrocardiography and two-dimensional echocardiography, and measurement of urinary microalbumin excretion were also carried out. No relation was found between blood pressure determined by clinic or ambulatory sphygmomanometry and retinopathy. The retinal features sought on fundal photographs were the percentages of arteriovenous crossings with venule nipping, venule deviation, or attenuation of venular light reflex. The ratio of arteriolar to venular diameter was measured. Only focal narrowing of arterioles was associated with higher blood pressure. There was no independent relation between retinal features and age, measures of left ventricular mass, or urinary microalbumin excretion. Assessment of arteriovenous crossing abnormalities by direct ophthalmoscopy was subject to wide variability among the panel members. Direct ophthalmoscopy was not clinically useful in the assessment of mild to moderate hypertension, whereas urinary microalbumin excretion correlated strongly with clinic blood pressure.

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The effects of monotherapy with the angiotensin converting enzyme (ACE) inhibitor perindopril (8 mg once daily) on 24-h ambulatory intra-arterial blood pressure, forearm blood flow, left ventricular mass, vasoactive hormones and cardiovascular reflexes were determined in eight hypertensive patients using a randomized, double blind, placebo-controlled, cross-over protocol. Six weeks of perindopril treatment was associated with a significant reduction of ambulatory blood pressure and a significant increase in forearm blood flow. Whilst the haemodynamic responses to Valsalva's manoeuvre, tilt, isometric forearm exercise and cold pressor testing were unaffected by perindopril, significant augmentation of the bradycardia during facial immersion was seen after chronic therapy. Sino-aortic baroreceptor-heart rate reflex resetting was apparent within 2 h of the first dose; this effect persisted throughout the active treatment period. Withdrawal of treatment was associated with a persisting hypotensive effect and an increase in heart rate which was not accompanied by an increase in plasma catecholamines. We conclude that perindopril, in a dose of 8 mg once daily, was an effective antihypertensive agent. We postulate that chronic therapy was associated with a sustained increase in parasympathetic tone.

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