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Dose-Dependent Acute Effects of Passive Smoking on Left Ventricular Cardiac Functions in Healthy Volunteers
  1. Mikail Yarlioglues, MD*,
  2. Mehmet Gungor Kaya, MD,
  3. Idris Ardic, MD,
  4. Orhan Dogdu, MD§,
  5. Hatice Yarlioglues, MD,
  6. Cemil Zencir, MD,
  7. Mehtap Ozdogru, MD**,
  8. Mahmut Akpek, MD,
  9. Haci Ahmet Kasapkara, MD††,
  10. Bahadir Sarli, MD‡‡,
  11. Mustafa Duran, MD‡‡,
  12. Ali Dogan, MD,
  13. Ibrahim Ozdogru, MD,
  14. Abdurrahman Oguzhan, MD
  1. From the *Department of Cardiology, Sorgun State Hospital, Yozgat, Turkey; †Department of Cardiology, School of Medicine, Erciyes University, Kayseri, Turkey; ‡Department of Cardiology, Cengiz Gökçek Gaziantep State Hospital, Gaziantep, Turkey; §Department of Cardiology, Yozgat State Hospital, Yozgat, Turkey; ∥Department of Physical Therapy and Rehabilitation, School of Medicine, Erciyes University, Kayseri, Turkey; ¶Department of Cardiology, Kahramanmaras State Hospital, Kahramanmaras, Turkey; **Department of Family Medicine, School of Medicine, Erciyes University, Kayseri, Turkey; ††Department of Cardiology, Diskapi Training and Research Hospital, Ankara, Turkey; and ‡‡Department of Cardiology, Kayseri Training and Research Hospital, Kayseri, Turkey.
  1. Received November 20, 2010, and in revised form September 19, 2011.
  2. Accepted for publication September 27, 2011.
  3. Reprints: Mikail Yarlioglues, MD, Department of Cardiology, Sorgun State Hospital, Sorgun, Yozgat, Turkey. E-mail: drmikailyar{at}gmail.com.

Abstract

Objective We have previously shown that acute passive smoking impaired left ventricular diastolic function in healthy volunteers. The aim of this study was to determine whether length of exposure and/or ambient smoke concentration is the key determinant of this outcome.

Methods We measured blood carboxyhemoglobin (COHb)and lactate level to investigate the acute effects of passive smoking on tissue oxygenation. A total of 90 healthy nonsmoker volunteers were prospectively enrolled into the study. Each of 30 subjects were exposed to carbon monoxide (CO) less than 5.0 ppm smoke in group A for 30 minutes, to CO 5 to 10 ppm smoke in group B for 30 minutes, and to CO less than 5.0 ppm smoke in group C for 60 minutes. Hemodynamic parameters were obtained, blood samples for measuring COHb and lactate levels were taken and echocardiographic examinations were performed at baseline and after exposure to passive smoking.

Results Mean ± SD CO levels in groups A, B, and C were 4.2 ± 0.5 ppm, 9.2 ± 0.3 ppm, and 4.1 ± 0.8 ppm, respectively. There was no change in left ventricular systolic functions in all groups. Left ventricular diastolic functions were impaired in groups B and C, whereas no change was observed in group A. Carboxyhemoglobin and lactate levels increased after passive smoking in groups B and C. However, group B had significantly higher COHb and lactate levels compared to group C (P < 0.001).

Conclusions Our results suggested that passive smoking at a certain dose in relation with length of exposure and ambient smoke concentration seems to cause relative left ventricular diastolic dysfunction.

Key Words
  • passive smoking
  • left ventricular diastolic function
  • length of exposure
  • ambient smoke concentration
  • carboxyhemoglobin levels
  • lactate levels

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