<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_218"
                     title="Even Mild COPD Affects the Heart (CME/CE)"
                     score="-0.002"
                     href="http://www.medpagetoday.com/Pulmonology/SmokingCOPD/tb/18070?impressionId=1265783710781"
                     
      Chronic lung disease begins to affect cardiac function at even mild levels of emphysema, data from a large prospective cohort study showed.&lt;br&gt;
&lt;br&gt;A 10-point increase in percent emphysema by lung CT had a linear inverse relationship with left ventricular end-diastolic volume (LVEDV), stroke volume, and cardiac output (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for all parameters), researchers reported in the Jan. 21 issue of the &lt;em&gt;New England Journal of Medicine&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;Current smoking status increased the magnitude of the association compared with former smokers and nonsmokers, the researchers found.&lt;br&gt;
&lt;br&gt;Left ventricular ejection fraction did not change with increasing percent of emphysema and airflow obstruction.&lt;br&gt;
&lt;br&gt;&quot;Previously, it has been well known that in very severe lung disease, the damage to the lungs affects heart function,&quot; lead author R. Graham Barr, MD, of Columbia University in New York, said in an interview.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;&quot;What we have shown is that a similar physiology, a similar relationship, would appear to extend up and down the spectrum of lung disease from mild, subclinical COPD and emphysema, all the way to moderately severe lung disease.&quot;&lt;/p&gt;
&lt;p&gt;Severe COPD can lead to cor pulmonale, characterized by increased vascular resistance and right heart failure, accompanied by reduced left ventricular filling, left ventricular stroke volume, and cardiac output.&lt;/p&gt;
&lt;p&gt;However, left ventricular ejection fraction (LVEF) usually is preserved. Whether similar changes occurred with less severe COPD had not been determined, and examining that question was the principal objective of the study by Barr and colleagues.&lt;/p&gt;
&lt;p&gt;The study population comprised a subgroup of patients enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA), which is exploring the prevalence, correlates, and progression of subclinical cardiovascular disease. The MESA Lung Study comprised 2,816 MESA participants who underwent cardiac MRI assessment of left ventricular structure and function.&lt;/p&gt;
&lt;p&gt;Investigators in the lung study excluded patients who had a restrictive pattern on spirometry, defined as a forced vital capacity (FVC) below the lower limit of normal and an FEV&lt;sub&gt;1&lt;/sub&gt;:FVC ratio &amp;gt;0.7.&lt;/p&gt;
&lt;p&gt;Information collected for the lung study included patient demographics, smoking history, medical history, level of physical activity, height, weight, resting blood pressure, serum glucose, C-reactive protein, and fibrinogen levels.&lt;/p&gt;
&lt;p&gt;Extent of emphysema was calculated from lung fields of cardiac CT scans, which included 70% of the lung volume from the carina to the base. Investigators defined extent of emphysema as the percentage of voxels below -910 Hounsfield units in the lung windows of cardiac CT scans.&lt;/p&gt;
&lt;p&gt;Participants who smoked at least one cigarette in the 30 days before CT or who had urinary cotinine levels &amp;gt;100 ng/mL were classified as current smokers.&lt;/p&gt;
&lt;p&gt;The mean age of the lung population was 61, and 51% were women. Current smokers accounted for 13% of the participants, former smokers for 38%, and nonsmokers for 49%. LVEF averaged about 70%.&lt;/p&gt;
&lt;p&gt;Mean spirometric measures were normal, as were measures of left ventricular structure and function. Median percent emphysema was 15%. Comparison of percent emphysema with left ventricular measures showed that a 10-point increase in percent emphysema was associated with a: &lt;ul&gt; &lt;li&gt;4.1 mL decrement in LVEDV&lt;/li&gt; &lt;li&gt;2.7 mL decrement in stroke volume&lt;/li&gt; &lt;li&gt;0.19 L/min decrement in cardiac output&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The investigators observed no evidence of an association between percent emphysema and LVEF, reflected in a 0.02-point mean increase with each 10-point increase in extent of emphysema.&lt;/p&gt;
&lt;p&gt;Smoking status significantly influenced associations of percent emphysema with LVEDV (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for interaction) and stroke volume (&lt;em&gt;P&lt;/em&gt;=0.008 for interaction).&lt;/p&gt;
&lt;p&gt;The magnitude of the association was greater among smokers than former smokers, and greater among former smokers than nonsmokers. However, the associations were evident in smokers and nonsmokers alike.&lt;/p&gt;
&lt;p&gt;&quot;The apparent effect of emphysema on left ventricular end-diastolic volume and cardiac output was similar to that of traditional cardiac risk factors previously reported in MESA and, among smokers, was greater than that of traditional cardiac risk factors,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;The linearity of associations across the study population &quot;suggests that even early-stage COPD influences stroke volume and left ventricular size,&quot; Anton Vonk-Noordegraaf, MD, of Vrije University Medical Center in Amsterdam, wrote in an accompanying editorial.&lt;/p&gt;
&lt;p&gt;&quot;Since oxygen delivery is directly related to cardiac output, a lower cardiac output in patients with COPD leads to impaired oxygen delivery,&quot; Vonk-Noordegraaf continued.&lt;/p&gt;
&lt;p&gt;&quot;Although the effects on cardiac output were small in this study population, they may be more pronounced in severe cases of emphysema and during exercise, as has been shown previously. The question is whether the striking clinical resemblance between COPD and chronic heart failure can be explained in part by a factor both diseases have in common: decreased cardiac output.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;Co-author Paul L. Enright disclosed relationships with Pfizer and Gilead.&lt;/p&gt;&lt;p&gt;Coauthor Eric A. Hoffman disclosed relationships with VIDA Diagnostics, sanofi-aventis, AstraZeneca, and Chiesi Pharmaceuticals.&lt;/p&gt;&lt;p&gt;Coauthor Kawut disclosed a relationship with Pfizer.&lt;/p&gt;&lt;p&gt;Co-author Jo&amp;#227;o A. C. Lima disclosed relationships with Toshiba Medical Systems and General Electric.&lt;/p&gt;&lt;p&gt;Co-author Lewis J. Smith disclosed relationships with Merck and KarmelSonix.&lt;/p&gt;&lt;p&gt;Vonk-Noordegraaf had no disclosures.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20090101_19_1003"
                     title="ACC: Resynch Therapy Slows Progress of Mild Heart Failure"
                     score="-0.005"
                     href="http://www.medpagetoday.com/MeetingCoverage/ACC/tb/13538?impressionId=1265783710781"
                     
       ORLANDO, March 31 -- Adding a biventricular pacemaker to optimal therapy for class I or II heart failure slowed progression of the disease more than medication alone, a randomized trial showed.
              &lt;p&gt; 
              &lt;p&gt;Among patients implanted with cardiac resynchronization devices, those with activated devices were significantly less likely to meet a composite endpoint that indicates worsening heart failure after two years (19% versus 34%, &lt;em&gt;P&lt;/em&gt;=0.01), according to Jean-Claude Daubert, M.D., of Centre Hospitalier Universitaire in Rennes, France.
              &lt;p&gt; 
              &lt;p&gt;He presented the findings at the American College of Cardiology meeting here.
              &lt;p&gt; 
              &lt;p&gt;The results came from the two-year follow-up of the European cohort of the REVERSE trial (Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction). The original analysis found that at one year, among patients in both North America and Europe, cardiac resynchronization therapy did not slow worsening of heart failure.
              &lt;p&gt; 
              &lt;p&gt;The one-year results did, however, demonstrate significant improvements in left ventricular function and reductions in hospitalizations for heart failure. (See: &lt;a href=&quot;http://www.medpagetoday.com/MeetingCoverage/ACC/8988&quot;target=&quot;blank&quot;&gt;ACC: Resynchronization Therapy Found Beneficial in Milder Heart Failure&lt;/a&gt;)
              &lt;p&gt; 
              &lt;p&gt;These benefits persisted through two years in the European patients.
              &lt;p&gt; 
              &lt;p&gt;The study included patients with New York Heart Association (NYHA) class I or II heart failure who had a wide QRS (at least 120 ms), a left ventricular ejection fraction of 40% or less, and an enlarged left ventricle.
              &lt;p&gt; 
              &lt;p&gt;All patients had a cardiac resynchronization device implanted and, among the European patients, 80 were randomized to an active device and 82 to an inactive device. All received optimal medical therapy.
              &lt;p&gt; 
              &lt;p&gt;The primary endpoint was a composite of heart failure hospitalization, all-cause death, the need for reassignment to the other arm, worsening NYHA class, or a worsening of symptoms as perceived by the patient.
              &lt;p&gt; 
              &lt;p&gt;Although patients in both groups declined over time, the decline was attenuated in those with an active device (&lt;em&gt;P&lt;/em&gt;=0.01).
              &lt;p&gt; 
              &lt;p&gt;Improvement in left ventricular function was seen at six months with active therapy and persisted through the end of follow-up (&lt;em&gt;P&lt;/em&gt;&lt;0.0001), indicating substantial reverse remodeling.
              &lt;p&gt; 
              &lt;p&gt;Over two years, left ventricular ejection fraction improved significantly in the active group, rising 6.7% from baseline (&lt;em&gt;P&lt;/em&gt;&lt;0.0001).
              &lt;p&gt; 
              &lt;p&gt;The time to first hospitalization with heart failure or death was reduced by 62% in the active group (HR 0.38, 95% CI 0.20 to 0.73).
              &lt;p&gt; 
              &lt;p&gt;However, there were no improvements in functional outcomes, including quality of life (&lt;em&gt;P&lt;/em&gt;=0.62), six-minute walk distance (&lt;em&gt;P&lt;/em&gt;=0.57), and NYHA class (&lt;em&gt;P&lt;/em&gt;=0.17).
              &lt;p&gt; 
              &lt;p&gt;Cecilia Linde, M.D., Ph.D., of Karolinska University Hospital in Stockholm, the principle investigator of the study, said at a news conference that the lack of functional effect was not surprising.
              &lt;p&gt; 
              &lt;p&gt;The patients were starting out with either no or mild symptoms, she said, so a much longer follow-up period would be needed to observe functional effects.
              &lt;p&gt; 
              &lt;p&gt;About 11% of the study participants had serious complications related to the resynchronization devices, primarily resulting from the left ventricular lead during the first year and the right ventricular lead in the second.
              &lt;p&gt; 
              &lt;p&gt;Nevertheless, taking into consideration the goal of keeping patients with few heart failure symptoms from progressing, Dr. Linde said, &quot;the benefits outweigh the risk.&quot;
              &lt;p&gt; 
              &lt;p&gt;&quot;We did achieve clinical improvement, we did achieve substantial improvement in ventricular function, and thus we conclude that [cardiac resynchronization therapy] does modify disease progression in class I and II heart failure patients.&quot;
              &lt;p&gt; 
              &lt;p&gt;Dr. Linde said the she believes that the results will change clinical practice and that class I and II heart failure patients will be indicated for cardiac resynchronization therapy as long as they have poor left ventricular function and a wide QRS.
              &lt;p&gt; 
              &lt;p&gt;Richard Page, M.D., of the University of Washington Medical Center in Seattle, who served as a discussant at Dr. Daubert&apos;s presentation, expressed concern that there were no functional benefits from resynchronization therapy.
              &lt;p&gt; 
              &lt;p&gt;&quot;There is significant cost and there is significant complication that can occur with these devices,&quot; he said, &quot;and while we&apos;re seeing in this follow-up study in this individual population some difference in worsening, I&apos;m still having trouble being convinced in terms of true improvement in functional capacity.&quot;
              &lt;p&gt; 
              &lt;p&gt;&lt;table cellspacing=&quot;0&quot; hspace=&quot;1&quot; style=&quot;border-style:solid; border-width:1px; border-color:#8dabbc; font-family:arial; font-size:12px; background-color:#DBE9F2; padding:5px 5px 5px 5px;&quot;&gt;
&lt;tr&gt;&lt;td&gt; The study was sponsored by Medtronic.
              &lt;p&gt; 
              &lt;p&gt;Dr. Daubert reported receiving consulting fees or honoraria from CV Therapeutics, Boston Scientific, CryoCor, Medtronic, Sorin Group, and St. Jude Medical, research grants from Boston Scientific, and fellowship support from St. Jude Medical, Medtronic, and Boston Scientific. He also reported having an equity interest in Medtronic.
              &lt;p&gt; 
              &lt;p&gt;Dr. Linde made no financial disclosures.
              &lt;p&gt; 
              &lt;p&gt;Dr. Page reported receiving consulting fees or honoraria from sanofi-aventis, and serving on the speakers&apos; bureaus of Astellas Pharma and Pfizer.&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
    </recommendedItem>
    <recommendedItem id="20090101_19_3713"
                     title="AHA: Heart Failure Linked to Poor Exercise Response (CME/CE)"
                     score="-0.005"
                     href="http://www.medpagetoday.com/MeetingCoverage/AHA/tb/17029?impressionId=1265783710781"
                     
      &lt;p&gt;ORLANDO  --  Heart failure patients with a normal left ventricular ejection fraction have an impaired heart rate response to exercise compared with healthy individuals, researchers found.&lt;/p&gt;
&lt;p&gt;They also have abnormal heart rate recovery after they&apos;ve finished exercising, Thanh Phan, MBChB, of the University of Birmingham in England, reported at the American Heart Association meeting here. The results were published simultaneously online in &lt;em&gt;Circulation: Heart Failure&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The findings are &quot;important because maximal heart rate response is associated with coronary disease and cardiovascular mortality,&quot; Phan and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;It will be important to undertake further studies to assess whether heart rate plays a causal role in exercise limitation in [these patients], because, if so, this may be amenable to rate responsive pacing,&quot; they said.&lt;/p&gt;
&lt;p&gt;About 50% of patients with clinical features of heart failure have a normal left ventricular ejection and valvular function, according to Phan and colleagues.&lt;/p&gt;
&lt;p&gt;These patients have similar hospitalization stays, admission rates, and mortality rate compared with patients with systolic heart failure.&lt;/p&gt;
&lt;p&gt;However, the prevalence of diastolic heart failure is increasing and the mortality rate is not declining, as with systolic heart failure, they said.&lt;/p&gt;
&lt;p&gt;A recent study of patients with heart failure with preserved left ventricular function found an association between an impaired heart rate response to exercise  --  called chronotropic incompetence  --  and exercise limitations, the researchers said.&lt;/p&gt;
&lt;p&gt;However, the study was limited in that most of the patients were black, the number of patients was small, and use of beta blockers was high.&lt;/p&gt;
&lt;p&gt;To explore the association in a larger sample, Phan and colleagues recruited patients who were not taking beta blockers and assessed their chronotropic response to exercise using maximal symptom limited erect treadmill metabolic exercise testing.&lt;/p&gt;
&lt;p&gt;The study included 41 patients with heart failure with preserved left ventricular function, 41 healthy controls, and 16 controls with hypertension, who were included to assess the possible contribution of high blood pressure to cardiac autonomic dysfunction.&lt;/p&gt;
&lt;p&gt;The participants were mostly female  --  70% for the heart failure group and 63% for the healthy controls  --  with mean ages of 69 and 67, respectively.&lt;/p&gt;
&lt;p&gt;Both groups had similar resting heart rate and predicted maximal heart rate.&lt;/p&gt;
&lt;p&gt;However, during peak exercise, the patients with heart failure had lower peak heart rate response and lower change in heart rate (60 versus 93) than the healthy controls (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for both).&lt;/p&gt;
&lt;p&gt;They also had significantly reduced peak oxygen consumption and a greater minute ventilation-carbon dioxide production relationship compared with the healthy controls (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for both).&lt;/p&gt;
&lt;p&gt;Chronotropic incompetence was significantly more common in patients with heart failure, according to both the portion of the heart rate reserve used during maximal exercise (63% of patients versus 2% of healthy controls) and the peak exercise heart rate as a percentage of the predicted maximal heart rate (34% of patients versus 2% of controls) (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for both).&lt;/p&gt;
&lt;p&gt;These rates were similar to those for patients with systolic heart failure.&lt;/p&gt;
&lt;p&gt;Abnormal heart rate recovery one minute after exercise had stopped was also more likely among patients in heart failure (23% versus 2%, &lt;em&gt;P&lt;/em&gt;=0.01), &quot;which suggests the presence of parasympathetic imbalance,&quot; the researchers said.&lt;/p&gt;
&lt;p&gt;The hypertensive controls were similar to healthy controls in in terms of chronotropic response to peak exercise and heart rate recovery following exercise.&lt;/p&gt;
&lt;p&gt;The researchers said the study was limited by the inability to use a control group of obese normotensive patients.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the British Heart Foundation.&lt;/p&gt;&lt;p&gt;One of Phan&apos;s co-authors reported receiving honoraria from Metronic, St. Jude, and Biotronik, serving as a consultant or member of the advisory board for Medtronic, St. Jude, Menarini, and Biotronik, and serving as a speaker for Menarini.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20090101_1_437"
                     title="U.S. Heart Failure Patients Have Better Short-Term Survival Than Canadians"
                     score="-0.005"
                     href="