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1. Systemic and renal haemodynamics, intravascular volume, circulating catecholamines and plasma renin activity were measured in 18 patients with established essential hypertension who were older than 60 years of age. Each patient was matched with respect to mean arterial pressure, body surface area, race and sex with a patient that was younger than 42 years of age. 2. When compared with the younger group, elderly patients had a lower cardiac output, impaired myocardial reserve, lesser aortic elasticity, higher total peripheral resistance, more contracted intravascular volume and higher circulating noradrenaline levels. 3. Similar effects of age, although less pronounced, have been reported in normotensive subjects. We conclude that essential hypertension is a pathophysiological process that seems to accelerate the natural physiological haemodynamic, fluid volume and endocrine processes of aging.

A 45-year-old male presented (February 2015) with a syncopal spell followed by sharp chest pain worsened with deep inspiration. The patient felt weak. Blood pressure (BP) was 90/46 with an increased pulsus paradoxus. The patient had elevated neck veins, and cardiac auscultation distant heart tones, but no murmur or rub. A bedside echocardiogram documented a moderate sized pericardial effusion (Fig. 1). An electrocardiogram revealed normal sinus rhythm (98 bpm) and a nonspecific repolarization pattern.Subsequently, the patient suddenly became unresponsive with a marked drop in BP with bradycardia. The patient received a saline challenge and underwent emergent pericardiocentesis with removal of 360 cc hemorrhagic fluid. Symptoms and hemodynamics improved. A catheter was left in place for drainage.Pertinent history included that of a dual chamber pacemaker implantation at another institution over twenty years prior (May 1994), for what was probably vasodepressor syncope. The patient was "lost" to follow-up. The device was a Medtronics Model 7076 pulse generator with a Telectronics Accufix J wire atrial lead (model 330-801) and Telectronics ventricular lead (model 4024-58).Over the course of the next day, the catheter continued to drain bloody fluid. Chest gated computed tomography (CT) without contrast demonstrated protrusion of the atrial J retention wire. It appeared to protrude from its polyurethane insulation, from the superior vena cava into the ascending aorta (Fig. 2). Surgical exploration found the same (Fig. 3). The protruding part of the J retention lead wire was clipped (Fig. 4), and sutures placed in puncture holes in the superior vena cava (SVC) and ascending aorta. Because of the patient's unstable status at the time of surgery, the leads and generator were left in place. Postoperative fluoroscopy was performed revealing residual retained retention wire within the axial body of the atrial J lead.On admission, it was noted that the patient had a Medtronic pulse generator, but the pacer Figure 1. Bedside two-dimensional echocardiography. Apical four-chamber view demonstrates moderate sized pericardial effusion (arrow). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. 1720