Cardiovascular phenotype of young adults and angiotensinogen alleles.

OBJECTIVES AND DESIGN: Angiotensinogen (AGT) gene variants influence angiotensinogen plasma levels in children and young adults. The angiotensinogen promoter (-6)A variant facilitates gene transcription in human tissues and it has been associated with high blood pressure in older adults. A young adult population can be used as a model to study genotype/phenotype associations between AGT (-6) variants and cardiovascular variables. METHODS AND RESULTS: Anthropometric measurements, blood pressure and heart rate were taken in 422 white Caucasian students (mean age 23.5 years, SD 2.5 years). Family history for hypertension, physical activity and smoking history were evaluated. Left ventricular variables were measured by echocardiography. Carotid artery wall intimal-media thickness (IMT) was measured by high resolution sonography and digitalized morphometry. The AGT G(-6)A alleles were evaluated by mutagenically separated polymerase chain reaction controlled by direct sequencing. No significant associations were found between angiotensinogen genotype and blood pressure, cardiac variables [except for deceleration time in females which increased with the number of (-6)A alleles] and IMT. Allele frequencies were similar between the first and third tertile of blood pressure and left ventricular mass, and were also similar between negative or positive family history for hypertension (the last group having significantly higher systolic blood pressure in males, P = 0.04 and diastolic blood pressure in females, P < 0.01). Moreover, no relevant interaction on the cardiovascular variables was found between AGT genotype and body mass index. CONCLUSIONS: The angiotensinogen G(-6)A variants do not affect cardiovascular parameters in young adults, but an effect of this polymorphism on cardiovascular phenotype (and hypertension) in older adults cannot be excluded. Additional factors, associated with ageing, should be present to unleash the supposed unfavourable potential of the (-6)A angiotensinogen variant.

[Acute myocardial infarction following administration of a synthetic analog of prostaglandin E2 in a subject with an intramural course of the anterior intraventricular artery]. / Infarto miocardico acuto dopo somministrazione di un analogo di sintesi della prostaglandina E2 in soggetto con decorso intramurale dell'arteria interventricolare anteriore.

We report a case of acute myocardial infarction which occurred after administration of a synthetic analog of prostaglandin E2 (PGE2) for the voluntary interruption of pregnancy in a 31-year-old woman who had previously been asymptomatic, with myocardial bridging of the left anterior descending artery. The pathogenesis of the severe ischemia causing myocardial infarction and left ventricle aneurysm is quite unclear. The temporal connection is highly indicative of a causal relationship between the pharmacological effects of a synthetic PGE2 analog and coronary spasm responsible for severe ischemia. The hypothesis of endothelial dysfunction proximal to the intramyocardial artery tract and paradoxical vasoconstriction with platelet activation should be taken into consideration. A possible additional effect seems to be a horizontal coronary steal produced by the administration of PGE2 in the myocardium below the intramyocardial artery tract. It cannot be excluded that pharmacological doses of a synthetic analog of PGE2 may have inverted the vasoactive effects of the substance due to direct stimulation on the delivery of constrictive agonist factors.