CCB (uptodate 19.3)

 ¾²ÀÌ´Â °÷

l  stable angina pectoris if there are contraindications or adverse reactions to either beta blockers or nitrates or if symptoms are not well controlled with a combination of these agents.(BB¿¡ ¿ì¼±¼øÀ§¹Ð¸²) , ÈäÅëÁÙÀÓ

l  vasospastic angina

l  hypertension

l  hypertrophic cardiomyopathy

l  supraventricular arrhythmias

ACS¿¡¼­´Â ¿Ö ¾È¾²´Â°¡?

DHP AMI ȯÀÚ¿¡¼­ óÀ½¿¡´Â À̷лó periinfarct zone¿¡ necrosis¹üÀ§¸¦ ÁÙ¿©ÁÙ°ÍÀÌ¶ó °¡Á¤ÇÏ°í µµ¿òÀ» ÁÙ°ÍÀ̶ó°í »ý°¢Çϰí trial(short acting nifedipine)À» ÇßÀ¸³ª, ÇØº¸´Ï±î mortality Áõ°¡·Î ÀÌÁ¦ ¾È¾¸ ¿øÀÎ ¹Ýº¹µÈ ÀúÇ÷¾Ð°ú ±³°¨½Å°æÇ×ÁøÀ¸·Î »ý°¢µÊ

      2¼¼´ë CCB (amlodipine,felodipine) : AMI ¿¡ ¿¬±¸´Â ½ÃÇàµÈ °ÍÀÌ ¾ø°í, HF, stable anginaÀÇ ¿¬±¸¿¡¼­´Â À̵浵 ÇØ¾Çµµ ¾ø¾ú´Ù.

                                          ±×·¯³ª, AMIÀÇ HTNȯÀÚ¿¡¼­ BP°¡  BB , ACEI or ARB·Î Á¶ÀýµÇÁö ¾ÊÀ» ¶§ ¾²°í ÀÖ´Ù.

NDHP(limited role in preventing nonfatal reinfarction) :

   MDPIT trial (diltiazem À» after AMI ȯÀÚ¿¡°Ô ÁÖ°í 25°³¿ù f/u Çß´õ´Ï, »ç¸Á·ü Àç¹ß·ü Â÷ÀÌ ¾ø´õ¶ó) LV functionÁÁÀº ¼­ºê±×·ì¿¡¼­´Â cadiac event ÁÙ¿´´Ù. LV function¾ÈÁÁÀº ¼­ºê±×·ìÀº evet,»ç¸Á·ü Áõ°¡.

   INTERCEPT trial systolic HF¾ø´Â AMI onset 36-96½Ã°£¿¡ ½ÃÀÛ Diltiazem ÁÖ°í 6°³¿ùÈÄ f/u Â÷ÀÌ ¾ø´õ¶ó. ,

   A pilot study : early¿¡ diltiazem IV·Î ÁÖ´Ï »ç¸Á·ü, Àç°æ»ö·ü, ÀçÇãÇ÷ÀÌ ÁÙ¾ú´Ù.

   DAVIT II trial AMI 2ÁÖÈÄ¿¡ verapamil Á൵ »ç¸Á·ü, cadiac event Â÷ÀÌ ¾ø´õ¶ó. ¿ª½Ã LV function ÁÁÀº ±×·ì¿¡¼­´Â »ç¸Á·ü, event°¨¼Ò, LV function ³ª»Û ±×·ì¿¡¼­´Â Â÷ÀÌ ¾øÀ½

        BB°¡ contraIdxÀ̸鼭 LV dysfunction, HF, AV block ¾øÀ»¶§¸¸ BB´ë½Å¿¡ MI¿¡ ¾µ¼ö ÀÖ´Ù.(»ç¸Á·ü event rate³·Ãã)

        AF RVR, Af RVR À̸鼭 MI¿¡,  BB°¡ contraIdxÀ̸鼭 LV dysfunction, HF, AV block ¾øÀ»¶§¸¸ BB´ë½Å¿¡ ¾µ¼ö ÀÖ´Ù.

ACS °£´Ü¿ä¾à : amlodipine, felodipine Àº ACS¿¡¼­ ¾µÀÏÀÌ ¾ø´Âµ¥, Ç÷¾ÐÀÌ Á¶Àý¾ÈµÇ¸é Ãß°¡·Î ½áº¼¼ö ÀÖ´Ù.

                 NDHP ACS¿¡¼­ ¾µÀÏÀÌ ¾ø´Âµ¥, BB¸ø¾µ »óȲÀÌ°í ¹ÚÃâ·® ±¦ÂúÀ¸¸é ½áº¼¼ö ÀÖ°í, »ç¸Á·ü ¹× event rate¸¦ ³·Ãá´Ù.(ACS¿¡¼­´Â ACEI, BB¸¦ ²À¾´´Ù. CCB¸¦ °°ÀÌ ¾µ¼ö´Â ¾ø´Ù. ¿ì¼±¼øÀ§¹Ð¸² ³»»ý°¢)

HF¿¡¼­´Â

vasodilationÀ¸·Î afterload¸¦ ÁÙ¿©¼­ systolic HF¿¡ È¿°ú°¡ ÀÖÀ» °ÍÀ¸·Î ±â´ëµÇ¾úÀ¸³ª, ¿¬±¸ÀÇ °á°ú negative inotrphic È¿°ú·Î ÀÓ»óÀû ¾ÇÈ­µÊ

amlodipine, felodipine´Â HF, stable anginaÀÇ ¿¬±¸¿¡¼­´Â À̵浵 ÇØ¾Çµµ ¾ø¾ú´Ù . µû¶ó¼­ systolic HF°¡Áø ȯÀÚÀÇ °íÇ÷¾ÐÄ¡·á, anginaÄ¡·á¿¡ ¾ÈÀüÇÏ°Ô ¾µ ¼ö ÀÖ´Ù. ÇÏÁö¸¸, HTN¿¡¼­´Â ACE, BB¸¦ ¸ÕÀú ¾²°í, angina, Afib¿¡¼­´Â BB¸¦ ¸ÕÀú ½á¾ßÇÑ´Ù.

±×¿Ü DHP , NDHP ´Ù ¾È¾´´Ù.

HF°£´Ü¿ä¾à : HF¿¡¼­´Â ¾È¾²´Âµ¥, amlodipine, felodipineÀº HFȯÀÚ°¡ Ç÷¾ÐÁ¶ÀýÀÌ ¾ÈµÇ¸é Ãß°¡·Î ¾µ¼ö ÀÖ°Ú´Ù(³»»ý°¢)

 

 

DHP

potent vasodilators than either verapamil or diltiazem.

vasodilate coronary arteries

blockade of calcium influx as well as an increase the levels of nitric oxide and bradykinin;

They elicit a strong reflex beta-adrenergic response,

only a mild negative inotropic effect,

 

NDHP

verapamil

 angina : decreases myocardial oxygen demand( by negative ino, chrono, lower BP)

          HF¿¡¼­´Â HF¸¦ ¾ÇÈ­½Ãų¼ö ÀÖ´Ù(negative ino)

Changes in contractility are minimal in patients without heart disease

much less potent vasodilator than the dihydropyridines

 

Diltiazem 

a potent coronary but a mild arterial vasodilator

improved blood flow through coronary epicardial vessels, collaterals

lowering mean arterial pressure

depress sinus node automaticity and AV nodal conduction time

not a negative inotrope.

 

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·Î ¹æ½Ç Â÷´Ü ¹× ¼öÃà±â ½ÉºÎÀüÁõ ȯÀÚ¿¡°Ô´Â Á¶½ÉÇØ¼­ »ç¿ëÇÏ¿©¾ß ÇÑ´Ù. ¶ÇÇÑ °í·É ȯÀÚ¿¡°Ô º£

ŸÂ÷´ÜÁ¦¿Í º´¿ë Åõ¿©ÇÒ ¶§ ÁÖÀǰ¡ ÇÊ¿äÇÏ´Ù.

 

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