Impaired systemic arterial compliance in borderline hypertension

Arterial compliance was evaluated by pulse wave velocity, pulse pressure/stroke volume, and by an exponential analysis of the diastolic blood pressure decay curve in three groups of normotensive, borderline hypertensive, and established essential hypertensive patients. Two of the above three indices reflected significantly impaired arterial compliance in borderline hypertension, and all three indices were distinctly abnormal in patients with established hypertension. A close correlation among the three indices was observed in the entire study population. Multiple regression analysis indicated that age (p < 0.005), systolic (p < 0.005) and diastolic (p < 0.025) pressure were independent determinants of pulse wave velocity; other factors such as total peripheral resistance, pulse pressure, and stroke volume were not. We conclude that arterial compliance becomes impaired early in hypertensive cardiovascular disease at the time when arterial pressure may be only slightly elevated. Thus structural alteration of the arterial wall can be demonstrated in borderline hypertension. Age, systolic and, to a lesser degree, diastolic pressures are the best determinants of arterial compliance in large vessels and are therefore important risk factors for evolving systemic arterial disease in essential hypertension.     

Immediate hemodynamic effects of a new calcium-channel blocking agent (nitrendipine) in essential hypertension

The immediate hemodynamic effects of a new calcium-channel blocking agent nitrendipine were studied in 12 patients with mild established essential hypertension. According to the response to mean arterial pressure, patients were classified into responders (decrease greater than 10 mm Hg, 7 patients) and nonresponders (less than or equal to 10 mm Hg, 5 patients). The decrease in arterial pressure in responders was associated with a significant (p less than 0.01) decrease in total peripheral resistance and a significant (p less than 0.05) increase in heart rate, cardiac index, and left ventricular ejection rate. The plasma norepinephrine level was significantly (p less than 0.05) increased in the responders. The response to upright tilt was qualitatively similar to pretreatment values. Thus, nitrendipine lowered arterial pressure as a result of arteriolar dilatation associated with a reflexive increase in heart rate and cardiac index. These hemodynamic properties make the drug particularly apt for use in combination with beta-adrenergic blockade for the treatment of arterial hypertension.     

Experience with operative transluminal balloon-catheter dilatation of the coronary arteries

A technique is presented for hand dilatation of coronary artery segments not amenable to bypass with a balloon catheter. This technique is used in 8% of patients undergoing routine coronary artery bypass surgery. Problems with catheter design, although troublesome, have resulted in no adverse sequelae to the coronary arteries. Postoperative angiography has revealed a good result in 71% of the lesions dilated. The technique is simple, is performed under direct visualization, and has proved to be safe.     

Obesity in hypertension: How innocent a bystander?

Hypertension and obesity frequently coexist in the same patient. However, the two disorders disparately affect cardiovascular function and structure. The presence of obesity significantly affects hypertensive target organ involvement. On one hand, obesity may tend to mitigate the harmful effects of a chronically elevated total peripheral and renal vascular resistance and lessen end-organ damage such as nephrosclerosis in essential hypertension. However, since both obesity and hypertension increase cardiac workload, although by different mechanisms, their presence in the same patient results in a double burden to the left ventricle. Congestive heart failure, sudden death, and coronary heart disease are common sequelae of obesity hypertension. Weight loss reduces arterial pressure by a decrease in intravascular volume and cardiac output associated with a fall in sympathetic activity. Intervention in obesity hypertension diminishes the dual hemodynamic burden imposed on the heart and becomes therefore a major objective in the prevention and treatment of heart disease.     

Disparate cardiovascular effects of obesity and arterial hypertension

Since obesity and essential hypertension frequently coexist, a study was designed to analyze some of their cardiovascular effects. Twenty-eight obese patients, half of whom were normotensive and half with established hypertension, were matched for mean arterial pressure with 28 corresponding lean subjects. Systemic and renal hemodynamics, intravascular volume, plasma renin activity, and circulating catecholamine levels were measured. Obese patients had increased cardiac output (p less than 0.001), stroke volume (p less than 0.001), central blood volume (p less than 0.02), plasma and total blood volume (p less than 0.01), and decreased total peripheral resistance (p less than 0.001). In contrast, cardiac output, central blood volume, and stroke volume of hypertensive patients were normal, but they had increased total peripheral (p less than 0.001) and renal vascular resistance (p less than 0.001) and a contracted intravascular volume. Left ventricular stroke work was elevated to a similar level in obesity (p less than 0.001) and hypertension (p less than 0.02), but the increase was caused by an expanded stroke volume in the former and by an increase in systolic pressure in the latter. It is concluded that the disparate effects of obesity and hypertension on total peripheral resistance and intravascular volume counteract and may even offset each other. Thus, obesity may mitigate the effects of chronically elevated total peripheral resistance (and therefore end-organ damage) in essential hypertension. Since both entities affect the heart through different mechanisms, their presence in the same patient results in a double burden to the left ventricle, thereby gently enhancing the long-term risk of congestive failure.     

Racial differences in cardiac adaptation to essential hypertension determined by echocardiographic indexes

Epidemiologic data point to racial differences in cardiac adaptation to hypertension. In this study, echocardiography and measurement of systemic hemodynamics were performed in 30 black and 30 white patients with untreated essential hypertension. Each black patient was matched with a white patient for age, sex and mean arterial pressure. Wall thickness measurements were similar, but left ventricular mass index was significantly increased in blacks (probability [p] less than 0.05). There was a nonsignificant increase in the number of black patients with posterior wall thickness greater than 1.1 cm. Only in black patients was posterior wall thickness related to systolic (r = 0.45; p = 0.008) and diastolic (r = 0.44; p = 0.0042) pressure and to total peripheral resistance (r = 0.32; p less than 0.046). Thus, although ventricular wall thickness changes are similar in black and white patients, qualitative differences exist in the cardiac adaptive process to systemic hypertension.     

Early hypertension and cardiac work

Myocardial function and ventricular work in early essential hypertension were assessed by comparing systemic hemodynamics and echocardiographic data in 33 normotensive subjects and 38 hypertensive patients, all without left ventricular hypertrophy. External work (tension-time index and cardiac work) and internal work (fiber shortening velocity) were significantly increased in the patients with mild hypertension. Because factors other than blood pressure contribute to cardiac work, antihypertensive therapy must favorably affect both blood pressure and cardiac work.     

Hypertension and sudden death: Increased ventricular ectopic activity in left ventricular hypertrophy

The present study was designed to detect and quantify cardiac arrhythmias in hypertensive patients with left ventricular hypertrophy. Continuous ambulatory electrocardiographic tracings and arterial pressure were recorded for 24 hours in 14 normotensive subjects, 10 patients with established essential hypertension without left ventricular hypertrophy, and 16 hypertensive patients with left ventricular hypertrophy by electrocardiographic criteria. Urinary excretion of norepinephrine was simultaneously measured over four successive four-hour and one eight-hour period. Patients with left ventricular hypertrophy had significantly more ventricular (but not atrial) premature contractions than those without left ventricular hypertrophy or than normotensive subjects. Five patients with left ventricular hypertrophy had episodes of more than 30 premature ventricular contractions per minute. Higher-grade ventricular ectopic activity such as coupled premature ventricular contractions was seen in two, and multifocal premature ventricular contractions were seen in three in the group with left ventricular hypertrophy. No difference in urinary catecholamine excretion rates among the three groups was seen. Left ventricular hypertrophy has been shown to be an independent risk factor for sudden death and acute myocardial infarction. Electrocardiographic monitoring of patients with left ventricular hypertrophy allows identification of those who have the highest risk and, therefore, require the most aggressive therapeutic intervention.     

Measurement of atrial septal defect during cardiac catheterization. Experimental and clinical results

The size of experimental and clinical secundum atrial septal defects may be accurately measured during cardiac catheterization. The position of the defects in the septum and their distance from the aortic and mitral valves may also be ascertained. A balloon catheter inflated with radiopaque dye is used for the measurement. The volume of dye in the balloon has been correlated with its maximal diameter. Thus, a no. 8-10 French catheter filled with 10 ml of diatrizoate (50 percent) has a diameter of approximately 25 mm and a no. 8-22 French catheter filled with 40 ml of diatrizoate a diameter of approximately 43 mm. Persistent arrhythmias or other adverse effects of the procedure were not observed. There was a high correlation between balloon-measured atrial septal defects and those measured at necropsy in the animals or at operation in the patients. These measurements aid in determining whether an ostium secundum defect is of proper size and location to be closed transvenously and may also prove valuable in physiologic studies of atrial septal defects or other cardiac anomalies.     

Essential hypertension in black and white subjects. Hemodynamic findings and fluid volume state.

Systemic hemodynamics (cardiac output, intraarterial pressure, total peripheral resistance) and intravascular volume (plasma volume and red cell mass) were measured in a population of 126 black and white patients, 51 with borderline hypertension and 75 with established essential hypertension. The findings were compared with those in 29 age-matched normotensive control subjects of both races. The white patients with established hypertension demonstrated a faster heart rate than the black patients (less than 0.05); this difference was more pronounced during upright tilt (p less than 0.02). No significant difference in cardiac index, total peripheral resistance, plasma volume or total blood volume was found between the two racial populations. Cardiac index correlated directly with plasma and total blood volume in black patients (r = 0.32, p less than 0.05) and white patients (r = 0.35, p less than 0.001) as well as in the whole study population (r = 0.36, p less than 0.001). The regression lines were similar in the two races. Further, a negative correlation was observed between the total peripheral resistance and plasma volume (r = -0.31, p less than 0.001) or total blood volume (r = -0.34, p less than 0.001), and it was similar in both races (blacks r = -0.48, p less than 0.01; whites r = -0.25, p less than 0.05). Age correlated significantly with total peripheral resistance in the white patients (r = 0.35, p less than 0.001) and in the total study population (r = 0.28, p less than 0.001). We conclude that, for every given age or level of arterial pressure, systemic hemodynamics are similar for the black and white patients with essential hypertension. These data, therefore, do not support the clinical impression that basic pathophysiology and hypertensive vascular disease are different in the black patient with essential hypertension.     

Severe papillary muscle dysfunction substantiated by atrial pacing during cardiac catheterization.

A patient experienced episodic pulmonary edema accompanying nocturnal angina pectoris. The symptoms were provoked at cardiac catheterization by atrial pacing. Simultaneous onset of chest pain, shortness of breath, and sudden appearance of a large V wave in the pulmonary artery wedge pressure contour confirmed acute mitral valve regurgitation. Rapid reversal of these changes after nitroglycerin administration supported "papillary muscle dysfunction" as the explanation for these hemodynamic changes.     

Echocardiographic diastolic ventricular abnormality in hypertensive heart disease: Atrial emptying index

To analyze changes in left ventricular diastolic properties in hypertensive heart disease, the atrial emptying index was used to assess the rapid phase of diastolic filling of the left ventricle. Ten normal subjects (Group 1), 11 hypertensive patients without evidence of cardiac involvement (Group 2) and 10 hypertensive patients with echocardiographic evidence of left ventricular hypertrophy (Group 3) were compared using M mode echocardiography and systemic hemodynamic data. Where as cardiac index (dye-dilution method) and rate of circumferential fiber shortening (echocardiogram) were normal in all three groups, there was a progressive increase in left atrial index (p <0.001, Group 1 versus Group 2 and versus Group 3) and a progressive decrease in the atrial emptying index (p <0.001, Group 1 versus Group 2 and versus Group 3). No correlation existed between the atrial emptying index and the left atrial index, mean arterial pressure or total peripheral resistance in any of the three groups. These data suggest that rapid filling of the left ventricle is reduced early in hypertension, even before electrocardiographic or systolic echocardiographic abnormalities are detectable. The atrial emptying index therefore appears to be an early indicator of abnormalities of left ventricular diastolic compliance in uncomplicated hypertension.     

Continued gains in hypertension

Although a variety of vasodilator drugs produce acute hemodynamic Improvement in patients with severe chronic heart failure, long-term treatment with these agents may be associated with the development of drug tolerance and loss of initial beneficial effects. Five serial right heart catheterlzations in a 78 year old man with severe chronic heart failure due to idiopathic cardlomyopathy documented the development of hemodynamic and clinical tolerance to oral hydralazine and oral captopril after Initial responses were observed to both agents. However, sustained hemodynamic and clinical improvement by invasive testing was noted with minoxidil (20 mg orally twice daily) after 4 and 9 weeks of continuous therapy. These observations indicate that pharmacologic tolerance may occur with a variety of vasodilator drugs and may account for the failure of some patients to improve clinically with long-term therapy despite initial favorable hemodynamic effects. However, such tolerance seems to be drug-specific and, hence, its recognition in an individual patient does not preclude responsiveness to other vasodilator agents.     

Enalapril improves systemic and renal hemodynamics and allows regression of left ventricular mass in essential hypertension

Enalapril, a new angiotensin-converting enzyme inhibitor, is an effective antihypertensive agent for both renovascular and essential hypertension. It is structurally different from captopril in that it does not possess a sulfhydryl group. The systemic and renal hemodynamic, biochemical and cardiac adaptive changes induced by enalapril were studied in 8 patients with essential hypertension before and after 12 weeks of therapy. Mean arterial pressure decreased from 110 to 90 mm Hg (p less than 0.01), and this was mediated through a decrease in total peripheral resistance from 42 +/- 3 to 32 +/- 3 U (p less than 0.01). Cardiac index and heart rate did not change. Renal plasma flow was increased in 6 of 8 patients and renal vascular resistance decreased from 123 +/- 6 to 91 +/- 7 U (p less than 0.001). Left ventricular mass index decreased from a mean of 166 +/- 29 to 117 +/- 8 g/m2 (p less than 0.05) without impaired myocardial contractility. Thus, enalapril lowers arterial pressure by reducing total peripheral resistance without reflexive cardiac effects. It also has favorable hemodynamic effects on the kidney. This is the first report of regression of LV mass with this agent in man.     

Posttraumatic coarctation of the aorta. Diagnostic clues

A patient with posttraumatic rupture of the aorta presented without the typical findings of mediastinal widening on chest roentgenogram, shock or hemothorax. The findings of acquired coarctation, that is, reduced volume of the femoral pulses and blood pressure difference between the arms and legs, led to early performance of retrograde aortography and successful corrective surgery. The need for attention to these subtle clues of aortic rupture is stressed.     

Achievements in hypertension: A 25 year overview

Only 25 years ago, the field of hypertension was challenged by retrospective clinical data and epidemiologic information suggesting that an elevated arterial pressure is a major risk factor for enhanced cardiovascular morbidity and mortality. Not only was antihypertensive therapy looked on by many as dangerous and fraught with severe and undesirable side effects, but its validity in reversing the course of disease was not yet demonstrated. This review discusses the dramatic new information amassed over the past 25 years that points to the new physiologic and clinical concepts concerning hypertension. It considers impressive new diagnostic techniques and methods designed to identify secondary forms of hypertension and target organ involvement. In summary, it outlines the feasibility of reversing overall (and cardiovascular) morbidity and mortality with an array of antihypertensive agents that provide the therapeutic ability to suppress most pathophysiologic pressor mechanisms of hypertensive disease. The lesson is clear: hypertension provides the greatest available challenge to the new era of preventive cardiology in the 21st century.