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[Left ventricular insufficiency: systolic versus diastolic dysfunction].

Left ventricular failure has been subdivided into different forms. Systolic pump failure (= systolic dysfunction) and diastolic filling failure (= diastolic dysfunction) are important entities in the overall framework of heart failure. The clinical patterns of both are presented in light of 2 case reports: systolic dysfunction involves the combination of left ventricular failure, cardiomegaly and depressed systolic ejection fraction. Diastolic dysfunction is accompanied by pulmonary congestion in the presence of a normal or only slightly enlarged ventricle and a normal ejection fraction. Prognosis of systolic dysfunction is poor, with a 5-year survival rate of 40%, compared to 70% in patients with isolated diastolic dysfunction. Medical treatment of systolic dysfunction is based primarily on ACE-inhibitors followed by diuretics and digitalis. Betablockers in low doses and spironolactone can provide additional benefit. Calcium channel blockers are rarely indicated, due to their negative inotropic effects. In patients with diastolic dysfunction, however, they are the first choice because of their positive lusitropic effect on relaxation and ventricular filling. ACE-inhibitors are suitable in hypertensive heart disease, while diuretics and betablockers are second line drugs. Digitalis should be avoided since worsening of diastolic function may occur.

Cardiovascular Agents↗

Impact of systolic and diastolic blood pressure on ischemic vascular diseases in French-Canadian men from 1974 to 1990.

The relationships of systolic and diastolic blood pressure (BP) to ischemic heart disease (IHD), intermittent claudication (IC) and stroke were evaluated in 4385 men (aged 35 to 64 years in 1973) clinically free from these vascular diseases at entry and followed for 16 years. The mean of two readings measured in 1973-74 was used as the baseline BP. The cut-of for quintile 5 was systolic BP greater than 152 mmHg and diastolic BP greater than 92 mmHg. Relative risks (RR) were adjusted for main risk factors and calculated separately for systolic and diastolic BP. From 1974-90, 1120 first ischemic vascular events were documented: 792 IHD, 216 IC and 112 strokes. The incidences of each ischemic vascular disease increased, starting at quintile 4, for either systolic or diastolic BP. For systolic BP, the adjusted RR of quintile 5 compared with quintile 1 were 1.8 for IHD (95% confidence interval 1.4 to 2.2), 2.7 for IC (1.8 to 4.2) and 3.8 for stroke (2.1 to 7.0); for diastolic BP, the RR were 1.8 for IHD (1.5 to 2.3), 1.5 for IC (1.0 to 2.1) and 3.5 for stroke (2.0 to 6.4). For IHD, the RR of BP were similar for angina and myocardial infarction, and more pronounced for coronary death. In this population, elevated BP constitutes an important risk factor not only for stroke, but also for the main manifestations of IHD and IC. The impact of systolic BP was at least as significant as that of diastolic BP on these ischemic vascular events.

Adult↗

Prevention of heart failure by antihypertensive drug treatment in older persons with isolated systolic hypertension. SHEP Cooperative Research Group.

CONTEXT: Heart failure is often preceded by isolated systolic hypertension, but the effectiveness of antihypertensive treatment in preventing heart failure is not known. OBJECTIVE: To assess the effect of diuretic-based antihypertensive stepped-care treatment on the occurrence of heart failure in older persons with isolated systolic hypertension. DESIGN: Analysis of data from a multicenter, randomized, double-blind, placebo-controlled clinical trial. PARTICIPANTS: A total of 4736 persons aged 60 years and older with systolic blood pressure between 160 and 219 mm Hg and diastolic blood pressure below 90 mm Hg who participated in the Systolic Hypertension in the Elderly Program (SHEP). INTERVENTION: Stepped-care antihypertensive drug therapy, in which the step 1 drug is chlorthalidone (12.5-25 mg) or matching placebo, and the step 2 drug is atenolol (25-50 mg) or matching placebo. MAIN OUTCOME MEASURES: Fatal and nonfatal heart failure. RESULTS: During an average of 4.5 years of follow-up, fatal or nonfatal heart failure occurred in 55 of 2365 patients randomized to active therapy and 105 of the 2371 patients randomized to placebo (relative risk [RR], 0.51; 95% confidence interval [CI], 0.37-0.71; P<.001; number needed to treat to prevent 1 event [NNT], 48). Among patients with a history of or electrocardiographic evidence of prior myocardial infarction (MI), the RR was 0.19 (95% CI, 0.06-0.53; P=.002; NNT, 15). Older patients, men, and those with higher systolic blood pressure or a history of or electrocardiographic evidence of MI at baseline had higher risk of developing heart failure. CONCLUSION: In older persons with isolated systolic hypertension, stepped-care treatment based on low-dose chlorthalidone exerted a strong protective effect in preventing heart failure. Among patients with prior MI, an 80% risk reduction was observed.

Aged↗

[Relationship between systolic and diastolic function of the left ventricle in patients with impaired relaxation of the left ventricle without symptoms of heart failure. Attempt at quantitative estimation of diastolic function in the impaired relaxation stage].

UNLABELLED: Diastolic dysfunction of left ventricle appears very often in patients with coronary artery disease (CAD) and hypertension (HT) and is a main cause of heart failure in 30-40% of all cases. Relation between systolic and diastolic function of left ventricle (LV) is commonly known but not documented well enough. Moreover, no quantitative classification of diastolic dysfunction is still available. AIM OF THE STUDY: To find out the relations between the parameters of systolic and diastolic function of LV in patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure and to make up the quantitative classification of diastolic dysfunction in the stage of impaired relaxation of LV. METHODS: Investigations were carried out in 57 patients (mean age 55.5 +/- 11.5) with angiographically proven CAD and in 91 patients (mean age 56.3 +/- 10.6) with HT and angiographically excluded CAD, all without regional myocardial contractility abnormalities and valvular heart diseases. Control group consisted of 54 healthy subjects (mean age 55.4 +/- 11.4). During 2D echocardiography examination left ventricular end-diastolic (LVEDD) and end-systolic diameters (LVESD) and left atrial dimension (LA) were obtained. Using Doppler method transmitral inflow indices: E velocity (E), A velocity (A), E velocity integral (E-VTI), A velocity integral (A-VTI), total velocity integral (T-VTI), E deceleration time (DT), isovolumic relaxation time (IVRT) and aortic flow velocity integral (Ao-VTI) were measured. Only patients with E/A < or = 1 and--to exclude pseudonormalization of mitral inflow--with DT > or = 140 ms were qualified to the study. We proposed diastolic dysfunction ratio (DDR) calculated from formula: DDR = E/A x E-VTI/T-VTI. Using AFVI, LV outflow diameter, heart rate (HR) and body surface area cardiac index (CI) was calculated. RESULTS: In studied group there were significantly higher values of LA, A, IVRT, DT and lower values of E, E/A, E-VTI and DDR compared to controls. There were no significant differences between these groups in HR, LVEDD, LVESD, T-VTI and CI. No significant differences in any of studied parameters were found between subgroups with CAD and HT. Among healthy subjects in subgroup with abnormal mitral inflow pattern (E/A < or = 1) there were significantly higher values of LA, IVRT, DT and lower values of DDR than in sugroup with normal one. Both subgroups did not differ in LVEDD, LVESD, CI. In the studied group there was positive correlation between DDR and CI (r = 0.69, p < 0.001), DDR and IVRT (r = 0.71, p < 0.001), DDR and DT (r = 0.61, p < 0.001), CI and E (r = 0.34, p < 0.01), CI and IVRT (r = 0.52, p < 0.001), CI and DT (r = 0.42, p < 0.001), CI and E/A (r = 0.54, p < 0.001), CI and E-VTI (r = 0.43, p < 0.001). In the control group significant correlation was found only between DDR and IVRT (r = 0.64, p < 0.02) and between DDR and DT (r = 0.52, p < 0.02) but not between DDR and CI. Using DDR DD was divided into 3 classes: class I with DDR > 0.47, class II with 0.47 > or = 0.30, and class III with DDR < 0.30. Applying of such intervals of values of DDR determined the groups which significantly differed between themselves in CI, IVRT and DT. CONCLUSIONS: (1) In patients with CAD or HT with impaired relaxation of LV without symptoms of heart failure there is relation between parameters of systolic and diastolic function of LV: the more advanced diastolic dysfunction, the more impaired systolic function. (2) In healthy subjects there is no relation between parameters of systolic and diastolic function of LV. (3) DDR is a good indicator of quantitative estimation of diastolic dysfunction in the stage of impaired relaxation of LV.

Adult↗

[Clinical study of effect of yinji capsule on left ventricular systolic function of angina pectoris patients with blood stasis syndrome].

OBJECTIVE: To explore the Yinji Capsule (YJC) in improving the left ventricular systolic function of angina pectoris patients with Blood Stasis Syndrome. METHODS: The systolic function of left ventricle (LV) in cardiac cycle of 28 angina pectoris patients with Blood Stasis Syndrome was examined with three-dimensional echocardiograph (3-DE) before and after treatment with YJC. RESULTS: The total symptomatic effective rate was 85.7%. The changes of LV systolic function were those: left ventricle ejection fraction (LVEF) increased from 45.0 +/- 4.9% to 48.2 +/- 3.5% (P < 0.05); EF on early stage and late stage increased from 22.6 +/- 2.1%, 8.3 +/- 1.2% to 28.1 +/- 3.0% and 10.3 +/- 0.9% respectively (P < 0.01, P < 0.05), myocardial region with segment systole (SS) < 5% decreased significantly (P < 0.01). CONCLUSION: YJC could improve LV systolic function on early stage and late stage in cardiac cycles, and mainly improve the systolic function of the region with low SS of LV.

Aged↗

Furosemide withdrawal improves postprandial hypotension in elderly patients with heart failure and preserved left ventricular systolic function.

OBJECTIVE: To assess the effects of furosemide withdrawal on postprandial blood pressure (BP) in elderly patients with heart failure and preserved left ventricular systolic function. METHODS: Noninvasive measurement of blood pressure (BP) and heart rate, computation of stroke volume and cardiac output (after a 1247-kJ (297-kcal) meal, and Doppler echocardiography before and 3 months after placebo-controlled withdrawal of furosemide therapy. RESULTS: Of 20 patients with heart failure (mean+/-SEM age, 75+/-1 years; left ventricular ejection fraction, 61%+/-3%), 13 were successfully able to discontinue furosemide therapy. At baseline, 11 (55%) of the 20 patients (had maximum postprandial systolic BP declines of 20 mm Hg or more. In the withdrawal group, the maximum systolic BP decline lessened from -25+/-4 to -11+/-2 mm Hg (P<.001) and the maximum diastolic BP from -18+/-3 to -9+/-1 mm Hg (P= .01), compared with no changes in the continuation group. In the withdrawal group, maximum postprandial declines in stroke volume and cardiac output decreased from -9+/-1 to -4+/-2 mL (P =.01) and from -0.6+/-0.2 to -0.2+/-0.1 L/min) (P = .04), respectively. The baseline maximum postprandial systolic BP decrease was correlated with the ratio of early to late flow (n = 20; Spearman rank correlation coefficient, 0.58; P = .007). For patients in the withdrawal group, the changes in postprandial systolic BP response were independently related to changes in peak velocity of early flow (n = 13; r2= 0.61; P = .003). CONCLUSIONS: Postprandial hypotension is common in elderly patients with heart failure and preserved left ventricular systolic function. The withdrawal of furosemide therapy ameliorates postprandial BP homeostasis in these patients, possibly by improving left ventricular diastolic filling.

Aged↗

The systolic arterial pressure/end-systolic volume relationship in patients with severe left ventricular dysfunction.

Performance of the intact left ventricle is well-defined by the end-systolic pressure/end-systolic volume relationship that appears independent of preload and afterload. To determine whether noninvasive measurements of this relationship could distinguish normal from abnormal subjects, we evaluated the relationship between arterial systolic pressure (determined by cuff sphygnomanometry) and radionuclide estimates of end-systolic volume in 12 normal subjects and 24 patients with severe left ventricular dysfunction. Data were acquired at rest, after atropine injection, and then during at least three increments of arterial pressure (average total increase approximately 45 mm Hg) using phenylephrine. The relationship between peak-systolic pressure (SP) and end-systolic volume (ESV) was found to be linear in all subjects (r greater than or equal to 0.91). The slope of this line was steeper in normal subjects than in myopathic patients (73 +/- 21.7 vs 20.8 +/- 8.7 mm Hg/volume unit/m2, P less than 0.001) and the zero pressure intercept also was greater (49.8 +/- 30 mm Hg vs 27.1 +/- 44.2 mm Hg, P less than 0.01). Similarly, resting ejection fraction (EF) was greater in the normals (0.71 +/- 0.88 vs 0.21 +/- 0.07% P less than 0.001) and end-diastolic volume (EDV) was smaller (4.14 +/- 0.88 vs 6.58 +/- 0.65 volume units, P less than 0.01). Systolic pressure/end-systolic volume relationship determined by these noninvasive methods was linear in both patients with severely reduced cardiac function and normal control subjects, clearly distinguishing normal from severely impaired left ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Intramyocardial pressure: effect of preload on transmural distribution of systolic coronary blood flow.

Impairment of systolic coronary blood flow (CBF) may be mediated by intramyocardial pressure (PIM). However, the effect of systole on the magnitude and transmural distribution of coronary blood flow has not been investigated. The purpose of this study was to measure this effect, and, indirectly, intramyocardial pressure. It is assumed that intramyocardial pressure acts on the coronary vessels as a Starling resistor, such that local coronary blood flow is determined by the equation: Coronary perfusion pressure minus intramyocardial pressure equals resistance times coronary blood flow. This equation was integrated with respect to time and solved simultaneously for intramyocardial pressure and resistance by measuring regional coronary blood flow (radioactive microsphere technique) during maximal coronary vasodilatation in two states: beating and hypocalcemic diastolic arrest. Measurements were made in 7 to 16 concentric layers of the left ventricle of 16 dogs. Intramyocardial pressure ranged from near zero to twice peak left ventricular pressure. The transmural distribution of intramyocardial pressure and systolic coronary blood flow depended on preload. The transmural distribution of the ratio of intramyocardial pressure to coronary perfusion pressure was not significantly different from unity across the left ventricular wall at low levels of preload (0 to 4 mm Hg). At moderate to high levels of preload (7 to 35 mm Hg) this ratio was not different from unity (mean 1.03 and 0.96) in the two inner fifths of the left ventricular wall, but was significantly lower (mean 0.79, 0.64 and 0.41, respectively) in the middle and two outer fifths. These data show that intramyocardial pressure shuts off systolic coronary blood flow across the entire left ventricular wall at low levels of preload, and at high levels of preload determines a gradient of decreasing systolic coronary blood flow from the subepicardium to zero in the subendocardial layers. This finding suggests that a dilated or failing left ventricle receives systolic flow to the outer myocardial layers, whereas at low preload levels myocardial perfusion occurs entirely during diastole.

Animals↗

Normal left ventricular systolic function in adults with atrial septal defect and left heart failure.

Systolic left ventricular contractile function has not been extensively evaluated in patients with atrial septal defect who have symptoms of left-sided congestive heart failure. This study examined left ventricular systolic function hemodynamically and angiographically in 6 such adult patients (Group A), 12 adult patients with atrial septal defect without heart failure (Group B) and 20 normal subjects. The mean ( +/- standard error of the mean) left ventricular end-diastolic pressure was higher in patients in Group A (17 +/- 0.8 mm Hg) than in patients in group B (6.9 +/- 0.6 mm Hg) (p less than 0.001). Both right atrial pressure ( 11 +/- 1.3 versus 4.9 +/- 0.5 mm Hg) (p less than 0.001) and mean pulmonary arterial pressure (30 +/- 1.8 versus 15 +/- 1 mm Hg) were also higher in Group A than in Group B. Left ventricular cardiac index and stroke work index did not differ in the two groups. Variables of left ventricular systolic function were similar in both groups of patients and in normal subjects: Ejection fraction was 0.71 +/- 0.05 in Group A, 0.74 +/- 0.02 in Group B and 0.74 +/- 0.01 in normal subjects. Velocity of circumferential shortening was 1.38 +/- 0.14 circumferences/s in Group A, 1.38 +/- 0.07 circumferences/s in Group B and 1.27 +/-0.04 circumferences/s in normal subjects. There was no difference in left ventricular contractile function as indicated by the ratio of end-systolic wall stress to end-systolic volume index among the three groups: normal subjects, average 5.6 +/- 0.19 versus 6.1 +/- 0.5 in Group B and 6.0 +/- 0.6 dynes X 10(3)/cm(2)/(ml/m(2) in Group A. This study of patients with atrial septal defect and left heart failure indicates that abnormal left ventricular systolic contractile function is probably not the cause of the symptoms and elevated left heart filling pressures observed in this group. An abnormality in left ventricular diastolic filling, perhaps related to the volume loaded right ventricle, may explain these changes.

Adolescent↗

Tricuspid stenosis. Atrial systolic murmur, tricuspid opening snap, and right atrial pressure pulse.

Observations on the atrial systolic murmur, the tricuspid opening snap, and the right atrial pressure pulse of tricuspid stenosis are presented, based on catheter manometer intracardiac sound and pressure recordings in five patients with hemodynamically significant tricuspid stenosis. The manometer-recorded right atrial pressure pulse of tricuspid stenosis differed from the normal, with (1) elevation of right atrial pressure, (2) different morphologic features (tall, spiky A wave complete before C; small V wave with an interruption, the tricuspid opening snap notch at termination of the gradual Y descent; a diastolic plateau, the relatively flat diastolic segment of the right atrial pressure pulse following the tricuspid opening snap notch prior to the next A wave), and (3) the relative lack of right atrial pressure and right atrial pressure pulse response with normal respiration. The atrial systolic murmur, recorded in the right ventricular inflow tract, was complete by S1; the crescendo-decrescendo atrial systolic murmur configuration paralleled the right ventricular-right atrial diastolic pressure gradient at the time of the atrial A wave. The right atrial contraction-relaxation process, as reflected by the right atrial A wave ascent and descent, was complete at the onset of ventricular systole with P-R intervals of 170 to 200 msec. Thus, the timing and configuration of the atrial systolic murmur reflected the timing and completion of the right atrial contraction-relaxation process prior to the onset of right ventricular systole and the configuration of the tricuspid diastolic pressure gradient. The tricuspid opening snap was recorded in the right ventricular inflow tract and occurred at the time of a notch at the termination of the Y descent of the right atrial pressure pulse V wave, while right atrial pressure exceeded right ventricular pressure. The sound-pressure events were consistent with angiographic and echocardiographic studies, which showed doming or ballooning of the mobile, fused, stenotic tricuspid valve into the right ventricle during the Y descent of the right atrial pressure pulse. The tricuspid opening snap occurred at the time of the termination of the diastolic movement of the fused tricuspid unit into the right ventricle. These observations are presented within the framework of previous studies in order to trace the development of medical ideas about the pathophysiologic basis for the sound and pressure events of tricuspid stenosis.

Adolescent↗

Epidemiology, pathophysiology, and management of isolated systolic hypertension in the elderly.

Isolated systolic hypertension (ISH) is a common disorder in the elderly, carrying with it a high risk of cardiovascular morbidity and mortality. Environmental and age-related factors believed to contribute to ISH include obesity, declining physical activity, stress, and such dietary changes as increased salt intake and decreased intake of calcium and potassium. Increased rigidity of the aorta resulting in reduced compliance is an important hemodynamic feature, but factors that increase peripheral resistance also appear to play a role. Antihypertensive drugs have been shown to effectively and safely lower the systolic blood pressure elevations characteristic of ISH. To date, use of low drug doses and careful titration of dosage have avoided significant orthostatic hypotension and undue lowering of the diastolic pressure. Studies of relatively small groups of patients suggest that antihypertensive drugs can lower the risk of cardiovascular morbidity/mortality associated with ISH but the definitive answer awaits results of the ongoing large-scale Systolic Hypertension in the Elderly Program trial. In the interim, management should begin with conservative measures such as weight loss, salt restriction and, possibly, calcium supplementation. If this fails, drug therapy should be considered in patients with systolic blood pressures above 180 mm Hg and in those with systolic readings between 160 and 180 mm Hg who have concomitant cardiovascular risk factors. To date, no controlled trials of sufficient size have demonstrated that one drug class is more effective than another in treating ISH. Drug therapy should be tailored to the individual patient, starting with a low dose of a single drug and, if necessary, slowly increasing dosage until a systolic blood pressure under 160 mm Hg is attained.

Adult↗

Exaggerated systolic blood pressure response to exercise: a normal variant or a hyperdynamic phase of essential hypertension?

This study examines the left ventricular function (by first-pass radionuclide angiography with a multicrystal gamma camera) at rest and during symptom-limited upright exercise in 27 normal subjects (group 1), 25 normotensive subjects with exaggerated systolic blood pressure response to exercise (greater than 200 mm Hg) (group 2) and 25 patients with essential hypertension and no associated coronary artery disease (group 3). There were no significant differences between groups 1 and 2 in exercise tolerance, heart rate, total vascular resistance, left ventricular ejection fraction and end-systolic volume. However, the exercise cardiac index and systolic blood pressure were significantly higher in group 2 (P less than 0.02). Compared to group 3, the subjects in group 2 had higher exercise heart rate (P less than 0.0001), cardiac index (P less than 0.0001), systolic blood pressure (P less than 0.0001) and left ventricular ejection fraction (P less than 0.0001) and lower exercise total vascular resistance (P less than 0.0002) and end-systolic volume (P less than 0.01). Thus, the hemodynamic profile in subjects with exaggerated systolic blood pressure response to exercise differs from that of essential hypertension; it may represent a supernormal response.

Adult↗

Intravenous contrast echocardiography with use of sonicated albumin in humans: systolic disappearance of left ventricular contrast after transpulmonary transmission.

The transmission of echocardiographic contrast medium and the cyclic changes in left ventricular videodensity during transpulmonary contrast echocardiography were investigated in nine adult volunteers with the use of intravenous injections of sonicated albumin (microbubble size 5.2 +/- 2.6 microns). Right and left ventricular and myocardial contrast were quantitated by videodensitometric analysis. The injections caused no symptoms, and no hemodynamic or electrocardiographic changes were observed. All injections resulted in right ventricular contrast. Mean peak right ventricular videodensity was 75 +/- 48 at end-diastole and 61 +/- 36 gray scale U/pixel at end-systole (p less than 0.05). Seventy-eight percent of injections resulted in left ventricular contrast with a mean peak videodensity of 21 +/- 33 gray scale U/pixel. Early systole was associated with a rapid decrease in left ventricular contrast intensity with near total disappearance of contrast by end-systole (from 23 +/- 33 and 17 +/- 23 U/pixel at end-diastole to 6 +/- 10 and 3 +/- 2 at end-systole at the left ventricular base and apex, respectively; p less than 0.05). None of the injections resulted in myocardial contrast enhancement by visual or quantitative analysis. Thus, left ventricular contrast echocardiography can be achieved after intravenous injections of sonicated albumin. Transpulmonary left ventricular contrast echocardiography is associated with near total disappearance of contrast during systole. This may be secondary to the destruction of microbubbles by the high left ventricular systolic pressure. These findings may help explain the limited success of this technique thus far for myocardial perfusion imaging.

Adult↗

Left ventricular systolic and diastolic function assessed with two-dimensional and doppler echocardiography in "white coat" hypertension.

OBJECTIVES: The aim of this study was to investigate left ventricular function in subjects with "white coat" hypertension, defined as office arterial diastolic pressure > or = 90 and ambulatory daytime pressures < 140/90 mm Hg. BACKGROUND: The white coat arterial pressure response may, by influencing left ventricular function, have a confounding effect in studies of heart disease. METHODS: Two-dimensional and Doppler echocardiography combined with the calibrated subclavian arterial pulse tracing, were used to assess variables of left ventricular function in 26 subjects with white coat hypertension (office arterial diastolic pressure > or = 90 and < 115 mm Hg and ambulatory daytime diastolic pressure > or = 90 mm Hg) and 32 normotensive subjects. RESULTS: In subjects with white coat hypertension, systolic arterial pressure during the echocardiographic examination was significantly higher than ambulatory daytime systolic pressure. This pressure response was positively related to the ratio of the systolic to diastolic pulmonary venous flow peak velocities and to the peak velocity of flow reversion during atrial systole; it was inversely related to the ratio of early to late mitral flow peak velocities. Left ventricular stroke volume, ejection fraction and velocity of circumferential fiber shortening did not differ in the study groups, but left ventricular external work and end-systolic wall stress were increased in the white coat group. CONCLUSIONS: The arterial pressure response in subjects with white coat hypertension is associated with increased left ventricular external work, increased end-systolic wall stress and alterations of left ventricular filling but normal ejection fraction and velocity of circumferential fiber shortening.

Blood Pressure↗

Is systolic blood pressure recovery after exercise a predictor of mortality?

BACKGROUND: An attenuated systolic blood pressure recovery after exercise has been associated with the severity of atherosclerotic heart disease. METHODS: For 6 years, we observed 12,379 patients who underwent symptom-limited exercise testing. We excluded patients receiving antihypertensive medication and patients with valvular disease, emphysema, end-stage renal disease, heart failure, left ventricular systolic dysfunction, and atrial fibrillation. Blood pressure recovery ratio was defined as the ratio of systolic blood pressure at 3 minutes into recovery to systolic blood pressure at peak exercise; this has been shown to correlate with angiographic severity of coronary disease. RESULTS: The blood pressure recovery ratios ranged from 0.36 to 1.62, with values for increasing quartiles of 0.72 +/- 0.05, 0.82 +/- 0.02, 0.88 +/- 0.02, and 0.99 +/- 0.07. During follow-up, there were 430 deaths (3%). Five-year Kaplan Meier survival rates were 0.975, 0.974, 0.969, and 0.966 in quartiles 1 to 4, respectively. Compared with patients in the lowest quartile of blood pressure recovery ratio, patients in the highest quartile were at somewhat increased risk (hazard ratio, 1.71; 95% CI, 1.31-2.24; P <.001). However, after adjusting for age, sex, body mass index, resting heart rate and blood pressure, peak systolic blood pressure, heart rate recovery, exercise chronotropic response, cardiac history, and standard risk factors, this association was no longer present (adjusted hazard ratio, 1.05; 95% CI, 0.8-1.38; P =.74). CONCLUSIONS: In this low-risk population, abnormal systolic blood pressure recovery after exercise was not independently predictive of mortality after correcting for differences in baseline and exercise characteristics.

Blood Pressure↗

Systolic blood pressure: it's time to take control.

Once considered an inconsequential part of the aging process, an age-associated rise in systolic blood pressure (SBP) occurs as a consequence of increased arterial stiffness and contributes to a high prevalence of systolic hypertension after middle-age. Elevated SBP imparts a predilection toward the onset of vascular events, highlighting the importance of its control. Current philosophy ranks systolic pressure as the most relevant component of blood pressure (BP) for determining risk for cardiovascular and other events in hypertensive patients, particularly those >50 years of age. Despite its prognostic role, SBP remains more difficult to control than diastolic BP (DBP), and most middle-age and older hypertensive patients fail to achieve recommended targets. In part, the lack of strict control of SBP in the more aged population lies in the physiology of hypertension. Younger persons tend toward isolated diastolic hypertension or combined systolic-diastolic hypertension, primarily driven by increased peripheral resistance and more effectively treated by antihypertensive medications; whereas older persons develop isolated systolic hypertension (ISH) associated with increased arterial stiffness that appears to be less amenable to current therapies. Thus, diastolic pressure in hypertensive patients often plateaus as patients reach middle-age and subsequently declines, whereas systolic pressure consistently rises through the ensuing decades. Treatment approaches favoring control of DBP frequently result in residual high SBP, putting patients at greater risk for vascular complications. Improving patient outcomes relies on antihypertensive therapy that appropriately addresses control of SBP and pulse pressure, underscoring the importance of therapeutic options that effectively reduce arterial stiffness.

Age Factors↗

Edge-to-edge technique to treat post-mitral valve repair systolic anterior motion and left ventricular outflow tract obstruction.

BACKGROUND: Systolic anterior motion of the mitral valve causing left ventricular outflow tract obstruction is an uncommon complication of mitral valve repair that may necessitate immediate additional surgical action. We prospectively evaluated the technique of the edge-to-edge suture on post-mitral repair systolic anterior motion, which persisted despite conservative treatment. METHODS: From March 2002 to March 2004, 4 of 112 patients requiring mitral valve repair surgery for chronic degenerative mitral regurgitation had systolic anterior motion with severe left ventricular outflow tract obstruction and mitral regurgitation. All 4 patients (mean age, 50 years) had posterior leaflet prolapse with chordal rupture with a billowing anterior leaflet, but without chordal rupture. Repair was achieved through a quadrangular resection of the posterior leaflet, completed by plication of the annulus in 2 patients and leaflet sliding in the other 2. All patients had mitral annuloplasty; two patients had a complete CE Physio ring (Edwards Lifesciences, Irvine, CA) inserted, whereas the other 2 patients had an open CG Future band (Medtronic, Minneapolis, MN). Routine perioperative transesophageal echocardiography showed systolic anterior motion, severe left ventricular outflow tract obstruction (> 50 mm Hg), and mitral regurgitation. After resuming cardiopulmonary bypass, all patients had an edge-to-edge suture at the middle part of the free edge of the anterior and posterior leaflets. RESULTS: The control transesophageal echocardiography showed in all cases disappearance of the systolic anterior motion, of the left ventricular outflow tract obstruction and of mitral regurgitation. Mean follow-up was 14 months (range, 6 to 28 months). All patients were in New York Heart Association's functional class I. CONCLUSIONS: With the edge-to-edge repair, the early and 2-year results were satisfactory with total disappearance of the systolic anterior motion, of the left ventricular outflow tract obstruction and of the recurrent mitral regurgitation.

Cardiopulmonary Bypass↗

Angina patients with diastolic versus systolic heart failure demonstrate comparable immediate and one-year benefit from enhanced external counterpulsation.

BACKGROUND: Enhanced external counterpulsation (EECP) is effective in treating angina in coronary artery disease patients. Whether EECP produces similar immediate and sustained benefits and freedom from adverse events (MACE) at 1 year in patients with severe systolic dysfunction versus diastolic dysfunction is unknown. METHODS AND RESULTS: Data of 746 angina patients with a history of heart failure enrolled in the International EECP Registry were divided into 2 groups: left ventricular ejection fraction (LVEF) < or =35% (S) and LVEF >35% (D). Mean LVEF was 51.0 +/- 10.2% in diastolic dysfunction (n=391) versus 26.3 +/- 6.9% in systolic dysfunction (n=355). At baseline, 92.0% of diastolic dysfunction and 90.9% of systolic had Canadian Cardiovascular Society Class III/IV angina with similar number of anginal episodes and nitroglycerin use. After 32 hours of EECP, angina was reduced by > or =1 class in 71.9% of diastolic versus 72.2% of systolic with similar decreases in anginal episodes and nitroglycerin use. At 1-year 78.1% of diastolic and 75.8% of systolic have less angina than pre-EECP. MACE at 1 year was also comparable (24.4 versus 23.8%). CONCLUSIONS: The benefits of EECP in heart failure patients were similar regardless of diastolic or systolic dysfunction. The improvement was sustained at 1 year with similar MACE.

Aged↗