Effect of Systolic and Diastolic Blood Pressure on Cardiovascular Outcomes.

BACKGROUND: The relationship between outpatient systolic and diastolic blood pressure and cardiovascular outcomes remains unclear and has been complicated by recently revised guidelines with two different thresholds (≥140/90 mm Hg and ≥130/80 mm Hg) for treating hypertension. METHODS: Using data from 1.3 million adults in a general outpatient population, we performed a multivariable Cox survival analysis to determine the effect of the burden of systolic and diastolic hypertension on a composite outcome of myocardial infarction, ischemic stroke, or hemorrhagic stroke over a period of 8 years. The analysis controlled for demographic characteristics and coexisting conditions. RESULTS: The burdens of systolic and diastolic hypertension each independently predicted adverse outcomes. In survival models, a continuous burden of systolic hypertension (≥140 mm Hg; hazard ratio per unit increase in z score, 1.18; 95% confidence interval [CI], 1.17 to 1.18) and diastolic hypertension (≥90 mm Hg; hazard ratio per unit increase in z score, 1.06; 95% CI, 1.06 to 1.07) independently predicted the composite outcome. Similar results were observed with the lower threshold of hypertension (≥130/80 mm Hg) and with systolic and diastolic blood pressures used as predictors without hypertension thresholds. A J-curve relation between diastolic blood pressure and outcomes was seen that was explained at least in part by age and other covariates and by a higher effect of systolic hypertension among persons in the lowest quartile of diastolic blood pressure. CONCLUSIONS: Although systolic blood-pressure elevation had a greater effect on outcomes, both systolic and diastolic hypertension independently influenced the risk of adverse cardiovascular events, regardless of the definition of hypertension (≥140/90 mm Hg or ≥130/80 mm Hg). (Funded by the Kaiser Permanente Northern California Community Benefit Program.).

Detection of paroxysmal atrial fibrillation by 30-day event monitoring in cryptogenic ischemic stroke: the Stroke and Monitoring for PAF in Real Time (SMART) Registry.

BACKGROUND AND PURPOSE: Patients with cryptogenic ischemic stroke may have undetected paroxysmal atrial fibrillation (PAF). We established the Stroke and Monitoring for PAF in Real Time (SMART) Registry to determine the yield of 30-day outpatient PAF monitoring in cryptogenic ischemic stroke. METHODS: The SMART Registry was a 3-year, prospective multicenter registry of 239 patients with cryptogenic ischemic stroke undergoing 30-day outpatient autotriggered PAF detection in Kaiser Permanente Northern California. RESULTS: In intention-to-monitor analysis, PAF was detected in 29 of 239 patients (12.1%; 95% CI, 8.6%-16.9%). After retrospective chart review was performed, a new diagnosis of PAF was confirmed in 26 of 236 patients (11.0%; 95% CI, 7.6%-15.7%). The majority of detected PAF events were asymptomatic; only 6 of 98 recorded PAF events (6.1%) were patient-triggered or associated with symptoms. CONCLUSIONS: -Approximately 1 in every 9 patients with cryptogenic ischemic stroke was found to have new PAF within 30 days. Routine monitoring in this population should be strongly considered.

Underdiagnosis of Isolated Systolic and Isolated Diastolic Hypertension.

Systolic and diastolic hypertension independently predict the risk of adverse cardiovascular events. It remains unclear how systolic pressure, diastolic pressure, and other patient characteristics influence the initial diagnosis of hypertension. Here, we use a cohort of 146,816 adults in a large healthcare system to examine how elevated systolic and/or diastolic blood pressure measurements influence initial diagnosis of hypertension and how other patient characteristics influence the diagnosis. Thirty-four percent of the cohort were diagnosed with hypertension within 1 year. In multivariable logistic regression of the diagnosis of hypertension, controlling for covariates, isolated systolic hypertensive measures (odds ratio [OR] 0.42 [95% confidence interval {CI} 0.41 to 0.43]) and isolated diastolic hypertensive measures (OR 0.32 [95% CI 0.31 to 0.33]) were less likely to lead to hypertension diagnosis when compared with combined hypertensive measures. Higher levels of systolic blood pressure had a greater impact on hypertension diagnosis (OR 1.77 [95% CI 1.75 to 1.79] per Z-score) than did higher levels of diastolic blood pressure (OR 1.34 [95% CI 1.32 to 1.36] per Z-score). Older age, non-white race/ethnicity, and medical comorbidities all predicted the establishment of a diagnosis of hypertension. Isolated systolic and isolated diastolic hypertension are underdiagnosed in clinical practice, and several patient-centered factors also strongly influence whether a diagnosis is made. In conclusion, our findings uncover a care gap that can be closed with increased attention to the independent influence of systolic and diastolic hypertension and the various patient-centered factors that may impact hypertension diagnosis.

Independent associations between electrocardiographic abnormalities and outcomes in patients with aneurysmal subarachnoid hemorrhage: findings from the intraoperative hypothermia aneurysm surgery trial.

BACKGROUND AND PURPOSE: Electrocardiographic abnormalities are common after subarachnoid hemorrhage, but their significance remains uncertain. The aim of this study was to determine whether any specific electrocardiographic abnormalities are independently associated with adverse neurological outcomes. METHODS: This was a substudy of the Intraoperative Hypothermia Aneurysm Surgery Trial, which was designed to determine whether intraoperative hypothermia would improve neurological outcome in patients with subarachnoid hemorrhage undergoing aneurysm surgery. The outcome was the 3-month Glasgow Outcome Score treated as both a categorical measure (Glasgow Outcome Score 1 [good outcome] to 5 [death]) and dichotomously (mortality/Glasgow Outcome Score 5 versus Glasgow Outcome Score 1 to 4). The predictor variables were preoperative electrocardiographic characteristics, including heart rate, corrected QT interval, and ST- and T-wave abnormalities. Univariate logistic regression was performed to screen for significant electrocardiographic variables, which were then tested for associations with the outcome by multivariate logistic regression adjusting for clinical covariates. RESULTS: The study included 588 patients, of whom 31 (5%) died. There was a significant, nonlinear association between heart rate and mortality such that lowest quartile (80 beats/min; OR, 8.8; P=0.006) were associated with higher risk. There was also a significant association between nonspecific ST- and T-wave abnormalities and mortality (OR, 3.1; P=0.031). CONCLUSIONS: Bradycardia, relative tachycardia, and nonspecific ST- and T-wave abnormalities are strongly and independently associated with 3-month mortality after subarachnoid hemorrhage. Further research should be performed to determine whether there is a causal relationship between cardiac dysfunction and neurological outcome after subarachnoid hemorrhage.

Acute neurocardiogenic injury after subarachnoid hemorrhage.

BACKGROUND: Left ventricular (LV) systolic dysfunction has been reported in humans with subarachnoid hemorrhage (SAH), and its underlying pathophysiology remains controversial. Possible mechanisms include myocardial ischemia versus excessive catecholamine release from sympathetic nerve terminals. METHODS AND RESULTS: For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[(123)I]iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to assess myocardial perfusion and sympathetic innervation, respectively. A blinded observer interpreted the scintigraphic images. Cardiac troponin I (cTI) was measured to quantify the degree of myocyte necrosis. Blinded observers calculated the LV ejection fraction and graded each LV segment as normal (score=1), hypokinetic (score=2), or akinetic (score=3). A wall-motion score was calculated by averaging the sum of the 16 segments. All subjects with interpretable scans (N=41) had normal MIBI uptake. Twelve subjects had either global (n=9) or regional (n=3) absence of MIBG uptake. In comparison with patients with normal MIBG uptake, those with evidence of functional denervation were more likely to have LV regional wall-motion abnormalities (92% versus 52%, P=0.030) and cTI levels >1 microg/L (58% versus 21%, P=0.029). CONCLUSIONS: LV systolic dysfunction in humans with SAH is associated with normal myocardial perfusion and abnormal sympathetic innervation. These findings may be explained by excessive release of norepinephrine from myocardial sympathetic nerves, which could damage both myocytes and nerve terminals.

Plasma B-type natriuretic peptide levels are associated with early cardiac dysfunction after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Serum B-type natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), as well as in the setting of congestive heart failure and myocardial infarction. The aim of this study was to prospectively quantify the relationship between BNP levels and cardiac outcomes after SAH. METHODS: Plasma was collected for BNP measurements as soon as possible after enrollment; a mean of 5+/-4 days after SAH symptom onset. On days 1, 3, and 6 after enrollment, troponin I (cTi) was measured and 2-dimensional echocardiography was performed. The following cardiac variables were collected and treated dichotomously: left ventricular ejection fraction (LVEF), regional wall motion abnormalities (RWMA), diastolic dysfunction, pulmonary edema, and cTi. RESULTS: There were 57 subjects. The median BNP level was 141 pg/mL (range, 0.8 to 3330 pg/mL). Higher mean BNP levels were present in those with RWMA (550 versus 261 pg/mL; P=0.012), diastolic dysfunction (360 versus 44; P=0.011), pulmonary edema (719 versus 204; P=0.016), elevated cTi (662 versus 240; P=0.004), and LVEF <50% (644 versus 281; P=0.015). CONCLUSIONS: Early after SAH, elevated BNP levels are associated with myocardial necrosis, pulmonary edema, and both systolic and diastolic dysfunction of the left ventricle. These findings support the hypothesis that the heart releases BNP into the systemic circulation early after SAH.

Doppler-detected valve movement in aortic stenosis: a predictor of adverse outcome.

BACKGROUND: The absence of auscultatory aortic valve closure sound is associated with severe aortic stenosis. The absence of Doppler-derived aortic opening (Aop ) or closing (Acl ) may be a sign of advanced severe aortic stenosis. HYPOTHESIS: Absent Doppler-detected Aop or Acl transient is indicative of very severe aortic stenosis and is associated with adverse outcome. METHODS: A total of 118 consecutive patients with moderate (n = 63) or severe aortic stenosis (n = 55) were included. Aop and Acl signals were identified in a blinded fashion by continuous-wave Doppler. Patients with and without Aop and Acl were compared using χ(2) test for dichotomous variables and analysis of variance for continuous variables. The associations of Aop and Acl with aortic valve replacement were determined. RESULTS: Aop or Acl were absent in 22 of 118 patients. The absence of Aop or Acl was associated with echocardiographic parameters of severe aortic stenosis. The absence of Aop or Acl was associated with incident aortic valve replacement (36.4% vs 7.3%, respectively, P < 0.001). Even in patients with aortic valve area <1 cm(2) , the absence of Aop or Acl was still associated with increased rate of aortic valve replacement (42.1% vs 13.9%, respectively, P = 0.019) and provided incremental predictive value over peak velocity. CONCLUSIONS: In a typical population of patients with aortic stenosis, approximately 1 in 6 has no detectible aortic valve opening or closing Doppler signal. The absence of an Aop or Acl signal is a highly specific sign of severe aortic stenosis and is associated with incident aortic valve replacement.

Remote monitoring of implantable pacemakers: in-office setup significantly improves successful data transmission.

BACKGROUND: Remote wireless follow-up of implanted pacemakers (PM) has become an attractive method of follow-up. Although wireless PM follow-up has several advantages compared with transtelephonic and office-based follow-up, its utility depends on successful transmission. HYPOTHESIS: Initial in-office setup of wireless PM will improve transmission rate as compared with home setup. METHODS: A total of 202 consecutive patients from 2 medical centers were included in this retrospective study. Patients in the home setup group (N = 101) had traditional home setup of wireless PM, whereas patients in the in-office group (N = 101) had setup of PMs by allied health professionals during the postoperative office visit. Successful transmission was defined as successful initial wireless transmission of PM data by 2 months postimplant. RESULTS: Of the 101 patients in the home setup group, 22 (22%) patients had successful transmission. Of the 101 patients in the in-office group, 92 (91%) patients had successful transmission (P < 0.0001). Logistic regression analysis showed that that the in-office group was independently associated with successful transmission (odds ratio: 114.5; 95% confidence interval: 32.1-408.4; P < 0.0001). CONCLUSIONS: In patients implanted with PM capable of remote wireless data transmission, initial home setup of the wireless monitoring device was frequently unsuccessful. In-office PM setup was associated with a significantly higher rate of successful transmission.

Predictors of left ventricular regional wall motion abnormalities after subarachnoid hemorrhage.

INTRODUCTION: Cardiac abnormalities that have been reported after subarachnoid hemorrhage (SAH) include the release of cardiac biomarkers, electrocardiographic changes, and left ventricular (LV) systolic dysfunction. The mechanisms of cardiac dysfunction after SAH remain controversial. The aim of this study was to determine the prevalence of LV regional wall motion abnormalities (RWMA) after SAH and to quantify the independent effects of specific demographic and clinical variables in predicting the development of RWMA. METHODS: Three hundred patients hospitalized with SAH were prospectively studied with serial echocardiography. The primary outcome measure was the presence of RWMA. The predictor variables included the admission Hunt & Hess grade, age, gender, cardiac risk factors, aneurysm location, plasma catecholamine levels, cardiac troponin I (cTi) level, heart rate (HR), blood pressure, and phenylephrine dose. Univariate and multivariate logistic regression was performed with adjustment for serial measurements, reporting odds ratios (OR) and 95% confidence intervals (CI). RESULTS: In this study, 817 echocardiograms were analysed. RWMA were detected in 18% of those studied. The prevalence of RWMA in patients with Hunt & Hess grades 3 - 5 was 35%. Among patients with a peak cTi level greater than 1.0 m g/L, 65% had RWMA. Multivariate analysis demonstrated that high Hunt & Hess grade (OR 4.22 for grade 3 - 5 versus grade 1 - 2, p = 0.046), a cTi level greater than 1.0 microg/L (OR 10.47, p = 0.001), a history of prior cocaine or amphetamine use (OR 5.50, p = 0.037), and higher HR (OR 1.34 per 10 bpm increase, p = 0.024) were predictive of RWMA. CONCLUSIONS: RWMA were frequent after SAH. High-grade SAH, an elevation in cTi levels, a history of prior stimulant drug use, and tachycardia are independent predictors of RWMA.

Hypernatremia predicts adverse cardiovascular and neurological outcomes after SAH.

INTRODUCTION: Abnormalities of serum sodium are common after subarachnoid hemorrhage (SAH) and have been linked to poor outcome. This study analyzed whether abnormal serum sodium levels are associated with cardiac outcomes and mortality after subarachnoid hemorrhage (SAH). METHODS: In a prospective cohort study of SAH patients, the primary predictor variable was subjects' sodium level. Hypernatremia was defined as sodium >143 mmol/L and hyponatremia was <133 mmol/L. Cardiac troponin I (cTi) was measured and echocardiography was performed on three study days. Dichotomous outcome variables were cTi > 1.0 microg/L, left-ventricular ejection fraction (LVEF) <50%, presence (vs absence) of regional wall motion abnormalities (RWMA) of the LV, pulmonary edema, and death. Additional analyses studied the degree of hypernatremia and sodium supplementation, and the temporal relationship between hypernatremia and cardiac outcomes. RESULTS: The study included 214 subjects. Forty-eight subjects (22%) were hypernatremic on at least one study day, and 45 (21%) were hyponatremic. After multivariate adjustment, hypernatremia was an independent predictor of LVEF <50% (OR 4.7, CI 1.3-16.2, p = 0.015), elevated cTi (OR 3.7, CI 1.2-11.9, p = 0.028), and pulmonary edema (OR 4.1 CI 1.4-1.5, p = 0.008). It was not, however a statistically significant predictor of mortality (p = 0.075). CONCLUSION: In the acute period after SAH, hypernatremia is associated with adverse cardiac outcomes and death. SAH patients with hypernatremia should be monitored for evidence of cardiac dysfunction.

Cardiovascular predictors of in-patient mortality after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Whether cardiac dysfunction contributes to morbidity and mortality after subarachnoid hemorrhage (SAH) remains controversial. The objective of this study was to test the hypothesis that cardiovascular abnormalities are independently related to in-patient mortality after SAH. METHODS: This was a prospective cohort study of patients with aneurysmal SAH. Heart rate and blood pressure were measured, a blood sample was obtained, and echocardiography was performed on three study days, starting as soon after admission as possible. The cardiovascular predictor variables were heart rate, systolic blood pressure (SBP), cardiac troponin I (cTi) level, B-type natriuretic peptide (BNP) level, and left ventricular ejection fraction. The primary outcome measure was in-patient mortality. The association between each predictor variable and mortality was quantified by multivariate logistic regression, including relevant covariates and reporting odds ratios (OR) and 95% confidence intervals (CI). RESULTS: The study included 300 patients. An initial BNP level greater than 600 pg/mL was markedly associated with death (OR 37.7, p < 0.001). On the third study day (9.1 +/- 4.1 days after SAH symptom onset), a cTi level greater than 0.3 mg/L (OR 7.6, p = 0.002), a heart rate of 100 bpm or greater (OR 4.9, p = 0.009), and a SBP less than 130 mmHg (OR 6.7, p = 0.007) were significantly associated with death. CONCLUSIONS: Cardiovascular abnormalities are independent predictors of in-patient mortality after SAH. Though these effects may be explained by a reduction in cerebral perfusion pressure or other mechanisms, further research is required to determine whether or not they are causal in nature.

Neurogenic Cardiac Injury.

Cardiac injury may occur following many types of brain injury, although the most widely investigated form of neurocardiogenic injury is subarachnoid hemorrhage (SAH). Echocardiography may help prognosticate and aid in the treatment of SAH if left ventricular (LV) dysfunction is suspected or if troponin levels are elevated. Cardiac catheterization, however, is not routinely recommended in SAH patients with LV dysfunction and elevated troponin. The priority should be treatment of the underlying neurological condition, even in the setting of LV dysfunction. Cardiac injury that occurs following an SAH appears to be reversible. For patients that develop brain death cardiac evaluation under optimal conditions may help increase the donor pool.

Cardiac injury after subarachnoid hemorrhage is independent of the type of aneurysm therapy.

OBJECTIVE: Subarachnoid hemorrhage (SAH) is associated with cardiac injury and dysfunction. Whether aneurysm clipping versus coiling has a differential effect on the risk of troponin release and left ventricular (LV) dysfunction after SAH is unknown. It is hypothesized that aneurysm treatment does not affect the risk of developing cardiac injury and dysfunction. METHODS: The study included 172 consecutive SAH patients who underwent clipping (n = 109) or coiling (n = 63) aneurysm therapy. Hemodynamic data were collected, cardiac troponin I was measured, and echocardiography was performed on the 1st, 3rd, and 6th days after enrollment. A cardiac troponin I measurement of more than 1.0 microg/L was considered abnormal. For each echocardiographic examination, a blinded observer measured LV ejection fraction (abnormal if <50%) and quantified LV regional wall motion abnormalities. The incidence of cardiac outcomes in the treatment groups was compared using odds ratios (ORs). RESULTS: The coiled patients were older than the clipped patients (mean age, 59 +/- 13 yr versus 53 +/- 12 yr; t test, P < 0.001) and were more likely to have posterior aneurysms (33% versus 18%; chi(2) test, P = 0.019). There were no significant between-group differences in the risk of cardiac troponin I release (coil 21% versus clip 19%; OR = 0.89, P = 0.789), regional wall motion abnormalities (33% versus 28%; OR = 0.76, P = 0.422), or LV ejection fraction lower than 50% (16% versus 17%; OR = 1.06, P = 0.892). No patient died of cardiac causes (heart failure, myocardial infarction, or arrhythmia). CONCLUSION: Surgical and endovascular aneurysm therapies were associated with similar risks of cardiac injury and dysfunction after SAH. The presence of neurocardiogenic injury should not affect aneurysm treatment decisions.