In middle-aged and elderly patients, increased arterial stiffness and wave reflections are consistently and independently associated with impaired systolic and diastolic function and with functional limitations.

Phosphorylation of the calcium-transport ATPase of skeletal muscle sarcoplasmic reticulum by inorganic phosphate was investigated in the presence or absence of a calcium gradient. The maximum phosphoprotein formation in the presence of a calcium gradient at 20 degrees C and pH 7.0 is approximately 4 nmol/mg sarcoplasmic reticulum protein, but only between 2.4 and 2.8 nmol/mg protein in the absence of a calcium gradient, using Ionophore X-537 A or phospholipase-A-treated sarcoplasmic reticulum vesicles. Maximum phosphoprotein formation independent of calcium gradient at 20 degrees C and pH 6.2 is in the range of 3.6--4 nmol/mg protein. Half-maximum phosphoprotein formation dependent on calcium gradient was achieved with 0.1--0.2 mM free orthophosphate at 10 mM free magnesium or at 0.1--0.2 mM free magnesium at 10 mM free orthophosphate. Phosphoprotein formation independent of calcium gradient is in accordance with a model which assumes, firstly, the formation of a ternary complex of the ATPase protein with orthophosphate and magnesium (E . Pi . Mg) in equilibrium with the phosphoprotein (E-Pi . Mg) and, secondly, an interdependence of both ions in the formation of the ternary complex. The apparent equilibrium constant was 0.6 and the apparent dissociation constants KMg, KMg', KPi and KPi' were 8.8, 1.9, 7.2 and 1.5 mM respectively, assuming a total concentration of the phosphorylation site per enzyme of 7 nmol/mg protein.

Mechanical systole is prolonged and arterial wave reflections are increased in most patients with DD. Rapid non-invasive assessment of these parameters may aid in confirming or excluding DD.

This case report describes the devastating consequences of spontaneous coronary dissection in a 36 year old female patient who otherwise had a normal coronary arteriogram. Intravascular ultrasound showed coronary artery dissection and intramural haematoma at the left main stem coronary artery. Acute coronary syndrome developed and subsequently surgical revascularisation was performed successfully. Spontaneous coronary artery dissection is a rare and often fatal cause of ischaemic heart disease occurring predominantly in young or middle aged otherwise healthy patients. It is mostly recognised at postmortem examination in young victims of sudden death.1 The cause of and optimal management approach for this challenging condition are still being debated. [1][2][3][4][5][6][7][8][9][10] About 250 cases of spontaneous coronary artery dissection have been reported in the literature. Spontaneous coronary artery dissection is the result of an intramural haematoma in the media of the arterial wall that creates a false lumen. Expansion of this lumen through blood or clot accumulation leads to compression of the real lumen and to myocardial ischaemia.An intimal tear is only seldom observed. Most reports are of apparently healthy, young to middle aged patients (mean age 40 years) without overt risk for coronary artery disease and without severe coronary atheromatosis.2 More than 70% of the reported cases occurred in women.2 The aetiology remains uncertain. We present a case of a spontaneous coronary dissection in a 36 year old female patient involving the left main stem. The patient was admitted with acute coronary syndrome and ECG signs of anterior wall ischaemia. Despite optimised pharmacological treatment, recurrent ischaemia occurred. Subsequently, surgical revascularisation was performed successfully. CASE REPORTA previously fit 36 year old white woman was admitted with a one hour history of chest pain. Precordial discomfort started during housekeeping. The patient had a fairly unremarkable medical history. She had two healthy children. Pregnancy was excluded by b human chorionic gonadotropin testing. She used no oral contraceptives or illicit drugs. There was no history of hypertension but the patient was a current smoker (10 pack-years). On examination, her supine heart rate was 86 beats/min and blood pressure was 112/78 mm Hg. She had no clinical signs of Marfan's syndrome or heart failure. On admission to hospital, her ECG showed ST segment elevation in the precordial leads indicating acute anterior wall myocardial infarction. Cardiac enzymes were slightly increased (creatine kinase (CK)) 204 U/l, normal range , 145 U/l; CK-MB fraction 23 U/l; troponin T 0.09 ng/ml, normal range , 0.03 ng/ml). Echocardiography showed a region of akinesia confined to the anterior wall and the apex of the left ventricle. The left ventricular lateral wall showed hypokinesia. The chest radiograph was normal. The patient was treated with aspirin, enoxaparin, metoprolol, nitrates, and opiates for acute coronary syndrome. Thirty five minut...

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